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TOWSON / Biology / MBBB 470 / What are negative feedback, positive feedback, and feed-forward system

What are negative feedback, positive feedback, and feed-forward system

What are negative feedback, positive feedback, and feed-forward system

Description

School: Towson University
Department: Biology
Course: Advanced Physiology
Professor: Nelson
Term: Summer 2015
Tags: Physiology
Cost: 50
Name: Biol 470 Exam 1 Study Guide
Description: This covers everything that will be on the exam through enteric nervous system and gut microbiota. I will update it after we cover stress response
Uploaded: 09/25/2017
44 Pages 72 Views 2 Unlocks
Reviews


Review questions for homeostasis and control systems 


What are negative feedback, positive feedback, and feed-forward systems? what roles do they play in the body?



Fall 2017

∙ What is homeostasis? What is allostasis?

o Allostasis is the process of achieving stability through ehavioral and  physiological changes

 Uses endocrine system

 Autonomic nervous system

 Cytokines released by cells

o Homeostaiss is the process of maintaining a stable internal  environment

∙ What is dynamic equilibrium?  

o Stability maintained within a range

∙ What are negative feedback, positive feedback and feed-forward  systems? What roles do they play in the body (give some examples  of each)?

o Negative feedback is when the response is in the opposite direction of  the stimulus


What are the different functional parts of the nervous system?



 It promotes stability and uses dynamic equilibrium

 Examples include

∙ Blood pressure

o Positive feedback promotes a change in one direction

 Promotes instability and disease

 Examples include

∙ Labor If you want to learn more check out What is the bis income statement (parts)?
If you want to learn more check out What refers to a biological reaction in which a creature maintains it's internal environment in response to its external environmental ccondition?

∙ Blood clotting

∙ Fever If you want to learn more check out What is the meaning of seed germination?

∙ Depolarization of a membrane to create action potentials

o Feed-forward is when your body anticipates and reacts to a change  before it happens

 An example is digestion starts when you smell food

∙ What are the parts of a negative feedback loop?

o Set point


What is the difference between the parasympathetic and sympathetic systems?



o Error Signal

o Effector

o Controlled Variable

o Sensor  

∙ Compare/contrast nervous system control vs. endocrine system  control.

o Nervous System

 Short term

 Fast

 Uses neurotransmitters

 Irreversible

o Endocrine System

 Long term

 Slow

 Uses hormones

 Reversible

∙ What are the different functional parts of the nervous system? o Sensory receptor, integrator, effector

o Organizaiton:

o Afferent (sensory) division

 Tactile, visual, auditory, olfactory, pressure, chemistry If you want to learn more check out What refers to the different forms of the same element that contain equal numbers of protons but different numbers of neutrons, and hence have a different atomic mass?

o Integrative Division (usually CNS)

 Process information, creation of memory

o Efferent (motor) Division

 Respond to stimuli and direction from CNS

 Autonomic Nervous system

∙ Visceral response – organs, glands, smooth and cardiac  

muscle

∙ Parasympathetic – rest and digest

∙ Sympathetic – fight of flight

 Somatic Nervous System

∙ Skeletal muscle

∙ What is the difference between the parasympathetic and  sympathetic systems?

o Parasympathetic is when you are at rest and controls normal body  function Don't forget about the age old question of What is the study of human populations?

o Sympathetic is when you are under stress and only uses the necessary  systems (ex: stops digestion)

∙ Name the different neural circuits we covered in class and give an  example of each.

o Diverging circuit

 One neuron to many

 Motor neuron activating many muscle cells

o Converging Circuit

 Many neurons to one

 Rods in retina

∙ Many rods synapse to one cell, and many bipolar cells  

synapse with one ganglion cell

o Serial processing

 One neuron to one neuron

 Cones in eye

o Recurrent or Reverberating Circuit

 kind of like a feedback mechanism

 learning and memory

o Lateral inhibition

 Activates one, inhibits others

 Allows for discernment of edges or points of sensory input ∙ What is the primary controller of the endocrine system? o Hypothalamus

 Can be influenced by info coming rom the vertebral cortex or  limbic system

∙ What are the different classes of hormones and how do they differ  from one another in their ability to be stored, travel in the  bloodstream, interact with target cells and the type of response  from the target cell?

o Amino acid derived hormones Don't forget about the age old question of What are the actions by the government to achieve a goal. it determines who gets what, when, and how with what results?

 Derived from tyrosine and tryptophan

 Tyrosine forms catecholamines like dopamine, norepinephrine,  and epinephrine and thyroid hormones like T3 and T4

 Tryptophan forms melatonin

o Lipid derived hormones

 Cholesterol can form a steroid backbone

∙ Gonadal (testosterone, progerterone), adrenal cortex, and placental steroids formed

 Arachidonic acid forms prostaglandins, leucotrines, and  

thromboxins but they typically can’t act in endocrine function o Peptide hormones

 Derived form DNA – RNA – Protein

 Peptides, proteins, and glycoproteins

o Steroid and thyroid hormones (lipid derived and some amino acid  derived) hormones are hydrophobic so they travel through the  bloodstream with a hydrophilic transport protein until they get to the  target cell. Then they can pass through the plasma membrane and  bind to cytoplasmic receptors

 They cannot be made ahead of time and stored

o Catecholamines, melatonin, and peptide hormones are hydrophilic so  they can travel as free hormones in the bloodstream, but they can’t  pass through the cell membrane so they bind to a receptor and use a  second messenger for signaling

 Can be made ahead of time and stored  

∙ What is unique about the production of peptide hormones? o Peptides often aren’t produced in their final form

o Called a pre-propeptide

o The pre part of the pre-propeptide is a targeting signal for the Golgi  and is cleaved before the vesicle transport to the Golgi

o The propeptide goes through the Golgi and into a secretory vesicle  where the pro part is cleaved off. The pro part targets it for secretion  and both are in the secretory vesicle

o SNARE proteins are used in the secretion of the peptide

 SNARE protein attaches to the vesicle

∙ SNARE on the vesicle and tSNARES of the membrane and  they attach

 Calcium influx into the cell drive exocytosis

o Example of this include insulin and opiomelanocortin  

∙ What proteins are required for exocytosis of hormones from  vesicles?

o SNARE and tSNAREs

∙ What hormones need second messengers?

o Hydrophobic hormones like steroid and thyroid hormones

∙ What are the different types of hormone interactions? o Trophic

 Hormone functions to control secretion of another endocrine  gland

∙ Regulatory hormones from hypothalamus to anterior  

pituitary  

o Synergistic

 Hormones work together and have a greater effect than one  hormone

∙ Glucagon causes release of glucose stores. If epinephrine  is present, you get release of more glucose

o Permissive  

 One hormone enables action of a second hormone

∙ Secretion of epinephrine by adrenal medulla is partially  

dependent on release of cortisol

o Antagonistic

 One hormone produces an effect opposite of another hormone ∙ Insulin signals storage of glucose, glucagon causes  

release of glucose

∙ Define clearance with regard to hormones.

o The removal or inactivation of the hormone

o Clearance rate will determine the half life

o Some hormones have very short half life

 Few seconds to a few minutes

 Catecholamiens and peptide horomones

o Others have a long half-life

 Hours or days

 Steroid and thyroid hormones

∙ If they are bound to the hydrophilic carrier protein

∙ If free, they disappear very quickly

∙ What role does negative feedback play in hormone levels? o All hormones fall under some kind of negative feedback control to  regulate their release.  

o The production of a hormone can often also be used to decrease the  production of that hormone

o Negative feedback combined with clearance determines how much is  in the blood  

∙ Know the basic HPA pathway (we will cover this more in the stress  lecture 9/26). What is the primary hormone known as the stress  hormone?

o Happens during chronic stress

o Hypothalamus releases corticotropic releasing factor

o Stimulates pituitary to produce ACTH

o Adrenal cortex produces cortisol

o Will update after 9/20 lecture

Module 2: Memory and Learning – Review questions 

THE CEREBRAL CORTEX

∙ Where do we find the cerebral cortex?

o The dark, outside layer of the brain

∙ What three types of neurons are found there?  

o Granular Neurons

 Interneurons

 Some inhibitory, some excitatory

 Most found in sensory and motor cortexes

 Processing

o Pyramidal  

 Make up axon tracts, carrying sensory or motor information

 White matter (corpus callosum, tracts to/from spinal cord)

o Fusiform

 Make up axon tracts, carrying sensory or motor information

 White matter (corpus callosum, tracts to/from spinal cord)

∙ What is the reticular activating system? Where is it found? What is  its function?

o The RAS is responsible for constantly activating the cerebral cortex and is necessary for survival

o It includes the reticular excitatory area, the mesencephalon, the  hypothalamus, and the thalamus

o It is responsible for wakefulness, arousal, consciousness, and attention ∙ If damaged what can it lead to? Malfunction of the RAS is thought to  contribute to what? What types of drugs increase activity of the  RAS? What type slow it down?

o If damaged, a person can experience sleep disorders, narcolepsy,  Alzheimer’s and senility (the late stage of Alzheimer’s), or coma o Malfunction to the RAS can cause overactive or underactive RAS  function

 People with an overactive RAS are hyperactive, talk too much,  ad are very restless

 People with an underactive RAS could have ADD/ADHD, and  their RAS can’t keep up with sensory input

o Psychoactive drugs that increase RAS activity are Adderall, Cocaine,  and Caffeine

o Painkillers decrease RAS activity

∙ What two mechanisms are used to stimulate activity in the cerebral  cortex?

o Direct Stimulation

 Maintaining a background level of activity in wide areas of the  brain

o Activation of neurohormonal systems

 Release facilatory or inhibitory hormone-like neurotransmitters  to selected areas of the brain

∙ What is the reticular excitatory area?  

o Sends signals to the cerebral cortex and spinal chord  

o Signals down to the spinal cord

 Antigravity and postural muscle tone

 Spinal cord reflex activity

o Signals up to the cerebral cortex  

 Thalamus (where sensory info comes in)

∙ Rapidly transmitted signals and slow transmitted signals

o Activity levels determined by sensory input

o Positive feedback loop  

∙ Where do signals from the Reticular excitatory area go? What is the  function of these signals? Distinguish between the rapid signals and  slow signals that go to the thalamus. What determines activity  levels in the reticular excitatory area?

o Signals go down to the spinal chord

 Antigravity and postural muscle tone

 Spinal cord reflex activity

o Signals up to cerebral cortex

 Thalamus (sensory input)

∙ Rapidly transmitted signals

o Signaling lasts for a few milliseconds

o Release of acetylcholine

∙ Slow transmitted  

o Come from small neurons and small, slow axons

o Allows for a slow buildup of excitatory potential

∙ Inhibitory neurons release serotonin to decrease activity  

of the cerebral cortex

∙ Rapid versus slow signals determined by sensory input

∙ What is neurohormonal control? What are the four systems found in  the human brain – specifically what are the four hormones? What is  a basic function of each?

o 3 pathways- hormones released for different functions

o Norephinephrine: excitatory to cortex

o Dopamine: inhibitory to basal ganglia

 Parkinson’s disease

o Serotonin: Inhibitory to diencephalon, cortex, and spinal cord o Acetylcholine: excitatory to cortex, spinal cord

o Many other neurohonrmonal substances, including enkephains, GABA,  glutamate, epinephrine, histamine, endorphins  

∙ The major parts of the limbic system are the hypothalamus,  hippocampus and amygdala. What is the overall function of the  limbic system?  

o The main function of the limbic system is to aid in learning and  memory, as well as serve a purpose in emotional response and  behavior. It links other parts of the brain to the cerebral cortex.

∙ The hypothalamus communicates with what parts of the brain? What are the functions of the hypothalamus?

o Signals down

 Signals go to reticular areas

∙ Contributes to wakefulness and sleep

 Signals to autonomic nervous system

∙ Signal sympathetic or parasympathetic

o Signals Up

 To midbrain

 To cerebral cortex

 Associated with feeding behaviors and arousal responses

o Signals through the infundibulum

 To pituitary

∙ Releasing and inhibiting hormones

∙ What are the functions of the hippocampus?

o It is stimulated by sensory input and in turn distributes the information  to the thalamus, hypothalamus, and parts of the limbic system  Signals go through the fornix

o Emotional response

 Plays a role in emotional responses such as rage, pleasure, etc. o Plays a role in learning and memory

o Disorder of Hippocampus: Korsakoff’s syndrome

 Anterograde and retrograde amnesia

∙ Anterograde: can’t remember anything from before the  

damage occurred

 Retrograde

∙ Can’t form new memories, don’t remember anything new  after the damage

 Caused by toxicity of alcohol or vitamin B deficiency

 Hippocampus and papaz circuit especially susceptible to  

damage

∙ What are the functions of the amygdala? If the amygdala is damaged or removed what results?  

o Plays a role in processing olfactory sensory information in humans and  lower animals

o In humans, it plays a role in behavior not associated with olfactory  stimuli

o Receives sensory input from auditory and visual areas

o Sends information to the limbic system

o Take home function: notifies limbic system of body’s current status in  relation to surroundings and patterns behavior and thought response o Kluver-Bucy Syndrome: loss of amygdala function

 Extreme curiosity

 Forget things rapidly

 Puts everything in mouth and swallow solid objects

 Extremely strong sex drive – try to mate with anything and  everything

∙ Where are the primary reward and punishment centers in the brain?  What role does reward and punishment play in learning and  memory?

o Reward centers are in the ventromedial nucleus and the lateral  hypothalamic area in the hypothalamus

o Punishment center found in the periventricular area in the  hypothalamus

o Reward and punishment are important in learning and memory  because if there is no reward or punishment associated with  

something, you won’t remember it  

 Habituation will occur without reward or punishment

∙ Continuous stimulation without reward or punishment

∙ Almost a complete lack of response by cerebral cortex

o With stimulation and a reward or punishment, there is a cortical  response and a memory is formed (typically long term memory) ∙ Define learning and memory. How are the two linked? o Learning is the process that will modify subsequent behavior o Memory is the ability to remember past experiences

o Memory is essential for learning because it serves as a record for the  learning process

o Learning also depends on memory because the knowledge stored  provides a framework to link new knowledge to  

∙ Describe the different types of memory. How long do they last? (I  don’t need specific times just a generalization)

o Sensory Memory

 Develops from sensory information

 Lasts 1 milisecond to 1 second

o Short Term Memory or Working Memory

 If you pay attention to the sensory memory, it becomes a short  term memory

 Lasts for about a minute

 Can only hold 7 things in your short term memory

o Long Term Memory

 Happens through encoding consolidation

 New synapses are formed

 Can last for days, months, years

 Memories that last for years are used often or are associated  with a strong emotion, reward, or punishment

 When you retrieve a long term memory, it is like a copy of it  goes to short term memory

∙ Describe the two types of long term memory and then the  subcategories (more general for the subcategories is fine). o Explicit (Declarative) Memory

 Knowing what – being able to describe a fact or event

 Semantic Explicit Memory –facts

 Episodic Explicit Memory – events

 Associated with temporal lobe, hippocampus, entorhinal cortex o Implicit (Non-declarative) Memory

 Knowing how to do something

 Procedural memory – skills and habits

 Classical Conditioning

∙ Skeletal musculature

∙ Emotional responses

 Priming

 Associated with cerebellum, and basal ganglia

∙ Define/describe what is meant by Encoding and  

Storage/Consolidation. What is important for consolidation to be  strong?

o Encoding

 Assigning a meaning to information to be learned

o Storage (consolidation)

 Converting short-term memory to a long term memory

 Rehearsal accelerated consolidation

 REM sleep helps consolidatoin

∙ What is retrieval? What is the difference between recall and  recognition?

o Retrieval

 Copying into short-term memory to use

o Recognition

 Only requires a decision as to whether you’ve seen the  

information before

 Activates only a few neurons

o Recall

 Actively restructuring all of the information from the memory  Activates all the neurons

∙ Why is Henry Molaison’s story important? What was removed and  what where the results? What does that tell us about that part of the brain (be specific)

o He had uncontrollable seizures and a very low quality of life, so doctors removed his hippocampus to stop seizures

o After the surgery, he couldn’t form new memories

 He lost explicit memory, but still had implicit memory

∙ Henry could learn to do new things that involved implicit  

memory, but he couldn’t remember that he knew how tot  

do them

o This was important because scientists were able to study what  functions the hippocampus really serve in creating and storing  memories

∙ What are the Aplysia good lab models for studying memory  formation?

o Aplysia are good lab models for studying memory formation because  they exhibit explicit memory and we can use classical conditioning and can habituate them  

o They can help us learn how other animals and humans form memories ∙ Define habituation? What happens at the neuron level during  habituation?

o Habituation is the decline in response due to repeated exposure to a  stimulus

o When habituation occurs, it is because less neurotransmitter are  released at the synapse

 It is not stored in memory because there is no reward or  

punishment associated with it

∙ Define sensitization? What happens at the neuron level during  sensitization?

o Sensitization is when there is increased or amplified response to all  stimuli

o This occurs because more neurotransmitter is released at the neurons  so there is a larger response to a stimuli

∙ What did Eric Kandel and his colleagues learn from their work with  Aplysia? Describe the basic experiments that they ran and their  findings. What is facilitation? Describe, in general, what happened at the cellular level during facilitation.

o Through their work with Aplysia, Kandel was able to study habituation  and sensitization, and therefore short term memory

o First, they saw if they touched the siphon, the gill pulled in a certain  amount

 If they continued to touch the siphon over and over again, the  gill eventually stopped retracting  

∙ Demonstrated habituation

o If they touched the siphon and then shocked the tail, the gill pulled all  the way in

 If they shocked the tail multiple times in a row, and then just  touched the siphon, the gill reacted as if it had been shocked ∙ Demonstrated sensitization

∙ Memory of the shock can last for up to 3 weeks

 They saw that this happened because the sensory neuron in the  tail synapses with a facilitating neuron that then synapses with  the motor neuron in 3 axoaxonal synapses

∙ Leads to increased neurotransmitter release at the  

synapses

∙ What is long-term potentiation? What is the role of LTP in learning  and memory?

o Long Term Potentiation is the process of making new/more proteins and new synaptic connections to form long term memories

o It is the process of release of glutamate and binding to AMPA and  NMDA receptors. That starts the process of forming new dendritic  spines and synaptic connections  

o Long term memories can’t be formed without long term potentiation ∙ Describe, in general, what happens at the cellular level during a  normal synaptic transmission and an LTP transmission. Why are they different? What role do the AMPA and NMDA receptors play? What is  the result of LTP physically? What ion is the most important in LTP? o During a normal synaptic transmission, there is the release of  glutamate from CA3, glutamate binds to the NMDA and AMPA  

receptors. There are low frequency action potentials

 AMPA channel opens, sodium enters, and there is a small  

depolarization of CA1

o During LTP, there are high frequency action potentials

 Release of glutamate from CA3 happens, and more is released  with increased Action Potentials

 Glutamate binds AMPA and NMDA receptors

 AMPA opens and a larger amount of sodium enters, so there is a  stronger depolarization

 Magnesium moves out of the NMDA channel and sodium and  large amounts of calcium enter the cell

 Calcium binds to calmodulin and enzymes are activated through  a second messenger pathway

 The calcium/calmodulin complex travels to the nucleus to  

activate gene transcription and translation of proteins like CREB  They also activate the formation of more NMDA and AMPA  

receptors that are inserted into the dendrite membrane

 More dendritic spines are built to increase synaptic connections o Normal synaptic transmission can create a sensory memory or short  term memory

o LTP creates a long term memory and alters the structure of the  dendrites

o Calcium is the most important ion in LTP

∙ What factors influence memory formation and retention? o Alertness, attentiveness, and concentration

o Interest, motivation, Need

o Mood, Emotion  

o Sensory stimuli

 Can increase memory function if it is linked to a sensory  

stimulus

 Enteric nervous system and gut microbiota Review  questions 

∙ What is the Gut-Brain or Brain-Gut Axis? What is its function?

o The Gut Brain is the enteric nervous system, which is the nervous  system in your digestive system

o It monitors and integrates gut functions

o It links emotional and cognitive parts of the digestive system  Immune system

 Enteric reflexes

 Intestinal permeability

 Enteroendocrine signaling  

∙ What functions do the CNS and the enteric nervous system have in  controlling digestive function? How do their roles differ?  o Enteric Nervous System

 Enteric nervous system controls the process of digestion  completely

 Input from the CNS doesn’t alter process of digestion, but can  alter when it occurs

o CNS

 Sympathetic nervous system can stop digestion in a stress or  fight or flight response

 Parasympathetic nervous system can start the process of  digestion through salivation when thinking about or smelling  food. This process is part of the CNS because food hasn’t  

entered the digestive system yet.  

∙ What are the enteroendocrine cells? What do they produce (in  general)?  

o They are endocrine cells specialized for the enteric nervous system o They produce GI hormones or peptides in response to stimuli o They travel in the blood, diffuse as local messengers, or activate  enteric nervous system cells

o Examples of secretions include somatostatin, gastrin, CCK, insulin,  glucagon, etc.  

o Long reflex: gets CNS involved

 CNS activates myenteric plexus  stretch receptrs,  

chemoreceptors, peristalsis

o Short reflex: just activates myenteric plexus, more localized ∙ There are many different types of neurons in the enteric nervous  system (ENS from here on), what are the ways they differ from one  another?

o Motor neurons

 Control secretory cells

o Interneurons

 Activate muscle, secretory glands, enteroendocrine cells

o Sensory Neurons

∙ What are the two nerve plexuses that make up the ENS? Where are  they located and what are their functions?

o Myenteric Plexus

 Between longitudinal and circular muscle layers

 Control movement in the GI tract

∙ Muscle control in the gut wall

∙ Intensity and velocity of peristalsis (pushing stuff through) ∙ Inhibitory actions by neurotransmitters

o VIP (vasoactive intestinal polypeptide) inhibits  

sphincter contraction to allow passage of chime

o Submucosal Plexus  

 Monitor lumen

 Regulate blood flow

 Control secretory cell function

 Lines small and large intestines

∙ We went over three connections between the CNS and the Gut:  Vagal, Thoracolumbar and Pelvic. For the first two, what component  of the Autonomic NS are they associated with. What type of sensory  and motor information would be carried in these axons (for all three  connections)?

o Vagal innervation is associated with the parasympathetic nervous  system

o Thoracolumbar innervation is associated with the sympathetic nervous  system

o Vagal

 Sensory/motor: esophagus, stomach, pancreas, small intestine,  proximal end of large intestines

 Sensory: lumen contents

∙ Indirect monitoring by chemoreceptors to detect nutrients and toxic substances

∙ Motor – same as myenteric plexus

o Thoracolumbar

∙ Digestion is controlled by long and short reflexes. What are the basic differences between the two?

o Long reflex

 Gets the CNS involved

 CNS activates myenteric plexus  stretch receptors,  

chemoreceptors, peristalsis

o Short reflex

 Just activates myenteric plexus

 More localized

∙ What are Hirschsprung’s and Chagas’ diseases? We compared these  to CNS damage with regard to digestive system function. Why are  the CNS related damage not as bad as the ENS?

o Hirschsprung’s Disease

 Distal ganglia of ENS fails to develop

 GI tract forms properly, but without innervation there is no way  to empty bowel

o Chagas’ disease

 Causes degeneration of ENS in colon, caused by infection of  protozoon trypanosome cruzi via bite by kissing bug

o CNS malfunction has only a minor effect on digestion because the ENS  is able to monitor digestion by itself.  

 You can cut the vagus nerve and still have proper digestion  ∙ Now the gut microbiota….

∙ Composition in the GI tract is determined by what factors? What  things can alter the composition? Are everyone’s gut microbiota the  same?

o Composition is determined by:

 Genetic factors

 Maternal health and well being

 Method of delivery

 Nutrition

 Maternal and postnatal exposure to antibiotics

o Composition can be altered by:

 Diet

 Pregnancy

 Transient microbiota through eating certain foods or taking  probiotics

 Exposure to antibiotics

∙ Are we born with the adult composition of microbiota? o No, microbiota diversity is small in newborns, it increases into  adulthood, and decreases again as we age.

∙ We can get transient bacteria (probiotics) from what types of foods? o Foods that are fermented such as:

 Yogurt

 Pickles

 Kimchi

 Sourdough bread

 Sauerkraut

 Miso

∙ Based on studies in humans and germ free mice, what are the  functions of the microbiota?  

o Development of innate and adaptive immunity

o Modulate Gut motility, intestinal barrier, absorption of nutrients o Influences stress reactivity and anxiety, regulate HPA set point o Important for proper brain and ENS development?

∙ We focused on germ free mice – how are they germ-free? What types of abnormalities are seen in these mice, associated with being germ free (some of these may overlap with the functions in the previous  question)?

o Germ-free mice are delivered by C-section and taken into a sterile  environment where they are not exposed to microbes

o Germ free mice had different GI structure development

 Enlarged secum, metabolic structural differences, reduced  intestinal surface area

o They had a higher susceptibility to infection  

 Reduction in pyerspatch area – less immune tissue

 Less lymphocytes in overall immune system

o They had memory problems

o They had alterations in the concentrations of neurotransmitters such  as serotonin  

 Serotonin is important in LTP, gut development, and ENS  

development  

∙ How do gut microbiota “communicate” with the CNS? o Production, expression and turnover of neurotransmitters (i.e.  serotonin, GABA) and neurotrophic factors (BDMF)

o Protection of intestinal barrier and tight junction integrity

o Modulation of enteric sensory afferents

o Bacterial Metabolites

o Mucosal immune regulation

∙ What is the function of the intestinal barrier? Why have tight  junctions? What happens when the integrity of the barrier is  reduced? What types of things cross into the body and what  happens as a result?

o We have outer and inner mucus layer to trap bacteria

o Epithelial cells are connected by tight junctions so nothing can leak  through the intestinal lining and into the blood

o Microbes maintain the tight junctions so that things don’t pass  between the epithelial cells

o Clostridium can break up the tight junctions  this causes diarrhea and  food poisoning symptoms  

o Stress can alter the tight junctions

o The leakiness of the epithelial cells when tight junctions are disrupted  causes unwanted materials to enter the blood stream

 Associated with celiac disease and IBS

o Bacterial metabolites can also cross into the body through  nonfunctioning tight junctions and interact with the CNS

∙ What are lipopolysaccharides? What are short-chain fatty acids?  What effects are seen when they leave the GI tract?

o Both are byproducts that are formed through bacterial metabolism o Lipopolysaccharides  

 Release inflammatory cytokines  

 Inflammatory cytokine release can interact with the  

enteroendocrine cells and stimulate the CNS and cause  

inflammation, activate immune system

 People with depression and chronic fatigue have high levels of  antibodies to lipopolysaccharides

o Short chain fatty acids

 Butynic acid, acetic acid

 Release stimulates the sympathetic nervous system

∙ Can lead to chronic stress

 Stimulates immune system/inflammation

 Can pass through the blood/brain battier and influence  

neurotransmitter production in the brain

∙ What cells make serontonin? We discussed serontonin when we did  learning and memory…what function does it have in that process? o Serotonin is made in the cells of the myenteric plexus  

o It can also be made by streptococcus  

 Serotonin is important for LTP

 Serotonin is released at the axoaxonal synapses and helps with  short term memory

o Serotonin is used in axoaxonal synapses. It is released from the  facilitating interneuron and is necessary for habituation and  

sensitization. Those processes are required in order to form memories. ∙ The gut microbiota may play roles in stress response, depression,  cognitive abilities, and behavior. Discuss the evidence we covered in  class for each. This could be based on human data, observations or  in germ free mice. I don’t expect you to know the exact microbes  that cause or alleviate symptoms, just a general idea of what is  known.

o Stress Response

 Gut microbes modulate normal stress response and activity of  HPA

 Germ free mice have an exaggerated stress response

 If within the first 6 weeks of life, bifidobacterium is introduced in  germ free mice, the stress response becomes normal  

 Stress in early life in normal mice causes release of cortisol,  activation of sympathetic and the stress response

∙ There were changes in microbe composition in these mice

o Depression

 The lipopolysaccharides and short chain fatty acids when  

released can lead to depression

 People with depression and chronic fatigue have high levels of  antibodies to lipopolysaccharides

o Cognitive Abilities

 Germ free mice have memory problems

 They have alterations in concentrations of neurotransmitters  such as serotonin

∙ Serotonin is important in LTP

o Behavior

 Cirrhosis of the liver causes the liver to not be able to filter  

things like microbes and microbe byproducts out of the blood

 People who have Hepatic Encephalopathy experience  

personality changes, but when treated with antibiotics, their  

personality returns to normal even though they don’t have an  

infection

 If microbes were taken from adventurous mice and put into shy  mice, they shy mice became adventurous  

Stress Review Questions

∙ What is the HPA axis? What does it control? What are the three  structures that make up the axis?

o Hypothalamic pituitary adrenal axis

o It controls the endocrine side of stress response and the overall release of cortisol through production of CRH and ACTH

o Hypothalamus, anterior pituitary, and adrenal cortex make up the axis ∙ What hormones are produced during a stress response? Which  glands secrete them and what do they do?

o The hypothalamus produces CRH (corticotrophin releasing hormone) o It then travels to the Anterior Pituitary were it signals for the  production of ACTH (adrenocorticotrophic hormone) by the anterior  pituitary

o ACTH travels to the Adrenal cortex where it signals for the production  of cortisol by the adrenal cortex

∙ How are levels regulated?

o Levels are regulated through a negative feedback loop

o Cortisol and ACTH provide negative feedback to the anterior pituitary  and hypothalamus to prevent the production of more CRH and ACTH ∙ What other hormone is released during a stress response? What role does it play?

o Vasopressin, or antidiuretic hormone is also released

o It goes to the posterior pituitary and makes sure you can respond to  other novel stressors

 If you are stressed about a test and the building catches on fire,  it makes sure you can respond to the new stress of the building  on fire

∙ Immediate alarm response is mediated by what system?  Neurotransmitter? What are some of the effects?

o Mediated by sympathetic nervous system

o Epinephrine is the neurotransmitter

o Effects include increased heart rate, increased ventilation, increased  vasoconstriction of specific regions such as skin, decreased digestion,  increased glucagon activity to break down glucose, increased fat  catabolism, and decreased insulin production to stop storing glucose

∙ The later or continued response is mediated by what system? What  hormones? What are the effects?

o Driven by the HPA axis

o CRH, ACTH, and cortisol are produced

o The actions of insulin are opposed, liver gluconeogenesis increased,  muscle/bone protein catabolism increases, Thyroid stimulating  hormone, gonadotropins, and growth hormones are inhibited, fat is  catabolized to free fatty acids and glycerol

∙ Cushing syndrome patients suffer from what? How does this help us  understand chronic stress?

∙ How does cortisol affect the ENS and what is the gut reaction to  stress?

o Cortisol inhibits digestion and activity of the ENS

o The ENS also has receptors for cortisol that when activated through  binding, contributes to stress response by the gut

∙ What does PGE2 do? What does this tell us about the immune  system and stress response?

o PGE2 is released by immune cells and it stimulates the zona fasciculata to produce more cortisol

o This tells us that the immune system increases stress response ∙ What do the studies on germ-free mice tell us about development of  the HPA axis and gut microbiota?

o Germ free mice have an exaggerated stress response

o However, if bifidobacterium are introduced within the first 6 weeks of  life, stress response is corrected and normal

o This suggests that the gut microbiota help with the development of a  normal functioning HPA axis, and the development is time sensitive –  developed within first 6 weeks of life  

∙ How does the limbic system influence stress response? What  functions do the hippocampus and amygdala play in HPA activity? o Most structures in the limbic system connect to the hypothalamus and  effect sympathetic output and HPA axis function  

o The have receptors to cortisol and can either inhibit or enhance stress  response

o The hippocampus will terminate HPA response to stress

 If hippocampus is activated by binding cortisol, it inhibits cortisol secretion

o The Amygdala will activate the HPA axis and promote cortisol secretion if it is activated

∙ What effect does chronic stress have on the hippocampus? Learning  and memory?

o Chronic stress can damage the hippocampus because of the high  cortisol levels  

o They can shrink the hippocampus and damage it  

o If the hippocampus is damaged, it hurts learning and memory  formation because the hippocampus is essential in forming long term  memories  

Recitation 

∙ Resting Membrane Potential

o Need a concentration gradient

o Need a selectively permeable membrane

o Need a mechanism to maintain the concentration gradient

o Na+ is high in ECF

o K+ is high in ICF

o Cl- is high in ECF

 Don’t see a lot of movement in because the negatives in the cell are up against the membrane, so if Cl- tries to go in, it is  

repelled

∙ Types of channels

o Resting (Leak) channels

 Always open

 We have many K+ leak channels, but few Na+ leak channels o Voltage Gated Chanel

 Opens in response to change in the membrane potential

o Ligand gated channel

 Opens in response to a specific extracellular neurotransmitter ∙ We maintain concentration through active transport with the  Sodium/Potassium ATPase pump.

o 3Na, 2K, 1ATP

∙ Membrane Potential

o Charge difference across the membrane

∙ Action Potential

o All axons aren’t the same – they may have different thresholds o Action potentials are all or none events that have the same amplitude  for all stimuli, weak or strong

o Frequency of Aps is quantitative data

 Always giving off constant signals for things like blood pressure – a change in frequency of Aps causes a response

o At resting membrane potential, voltage gated sodium and potassium  channels are closed and leak channels are open

o At threshold, voltage gated sodium channels opens and sodium flows  into the cell rapidly. Potassium also opens, but it opens very slowly o At the peak of depolarization, sodium channels close and potassium  channels are open all the way

o As the cell gets close to threshold again, the potassium channel starts  to close, but closes very slowly so the cell gets slightly hyperpolarized o At -40 mV the sodium channel resets

∙ Refractory period  

o During the absolute refractory period, you cannot stimulate another  action potential no matter how strong the stimulus

 Voltage gated sodium channels are already open or inactivated o During the relative refractory period, you can stimulate an action  potential but you need a stronger than normal stimulus

 During this period, there is a lot of K+ leaving the cell, so it  takes a lot of Na+ to overcome and bring the cell to threshold ∙ Conduction

o Conduction of current through a neuron occurs in 2 ways:

 Active regenerative conduction

∙ No decrement of signal

∙ Axons  

∙ Action potential

 Passive electronic conduction

∙ Depends on the physical properties of the cell

∙ Conduction degrades with time and distance

∙ Dendrites, soma, and some axons

∙ Local potential

∙ Unmyelinated regenerative conduction

o Each segment of the axon must depolarize and generate an AP ∙ Myelinated regenerative conduction

o Only have to depolarize the are in between the myelination o As the sodium comes in you have to make sure enough diffuses down  the axon to depolarize the next area, so myelination cant be too far  apart

∙ Cable properties of neurons

o Membrane resistance and internal resistance determine the length  constant of the membrane

o The length constant is the distance over which a membrane potential  will drop by 63%

o Myelinated axon = high Rm

o Large diameter = low Ri

∙ Types of synapses

o Axodendritic

 Axon to dendrite

o Axosomatic

 Axon to soma

o Axoaxonic

 Axon to axon

∙ Action potential

o Membrane of soma depolarized

o Voltage gated Ca2+ channels open

o Synaptic vesicles go to docking protein SNARE

o Neurotransmitter released and binds to receptor on neighboring  neuron

o Can have EPSP depending on what channel it binds to

 Excitatory

 Depolarizes membrane – local potential

 Sodium channels open

 Length constant determines signal

o Can have IPSP

 Inhibitory

 Hyperpolarizes membrane

 K+ or Cl- channels open

∙ Active zone

o Are on postsynaptic knob where vesicles bind to docking protein  ∙ For neuromuscular junction, it is always Ach released, it is always excitatory,  and we always reach threshold and send and AP

o If we didn’t want the muscle to contract, there would be no signal sent  at all

∙ General characteristics

o One way conduction

o Allows signals to be directed toward specific targets

o Over 40 substances identified as neurotransmitter

o Altered by amount of neurotransmitter available, pH of ECF, Ca2+ in  ECF, and drugs

o Neurotransmitters can be excitatory, inhibitory, or both depending on  the channel they bind

∙ How to get rid of neurotransmitter in synaptic cleft after AP stops o Some are taken back up through channel to be repackaged and reused o GABA can use reuptake, or it can be take up by an astrocyte, uses an  

enzyme to change it to glutamate, the another enzyme to change it to  glutamine, then brought back into cell where it is turned back to GABA o Ach is broken into choline and acetate. Acetate is processed out and  choline is taken back up where it combines with a new acetate from  mitochondria, is repackaged as Ach to be used again

∙ Synaptic Fatigue

o Happens when synapses are repetitively stimulated at a rapid rate  until neurotransmitter stores are depleted

∙ Long term facilitation

o Enhanced responsiveness following repetitive stimulation

o Mechanism is a build up of Ca2+ ions in the presynaptic terminals   Causes more vesicular release of neurotransmitter

∙ Long term depression

o Reduced responsiveness following low frequency stimulation o AMPA receptors removed from post synaptic cell

o Used in learning and memory

o Allows you to trim the network to make it more efficient  

o Without this you would run out of space for more dendritic spines to  form new memories

o Low frequency stimulation

o Glutamate binds receptors, sodium depolarizes membrane, calcium  comes in

o Instead of activating kinases, protein phosphatases are activated to  inhibit enzymes in pathway

o Can happen during LTP

∙ Temporal and spatial summation

o Temporal (time)

 When a second AP comes in before the sodium has left form the  1st AP, you can sum them together to cause a stronger  

depolarization to reach threshold

o Spatial (space)

 Aps from two different synapses can be summed together to  create a strong enough depolarization to reach threshold

∙ Drug Effects

o Agonistic

 Enhance synaptic activity

 Make more neurotransmitter

 Enhance release of neurotransmitter (more)  Drug binds to postsynaptic receptor

o Antagonistic

 Block synthesis of neurotransmitter

 Block release of neurotransmitter

 Block postsynaptic receptor

Review questions for homeostasis and control systems Fall 2017

• What is homeostasis? What is allostasis?

o Allostasis is the process of achieving stability through ehavioral and physiological  changes

▪ Uses endocrine system

▪ Autonomic nervous system

▪ Cytokines released by cells

o Homeostaiss is the process of maintaining a stable internal environment

• What is dynamic equilibrium?  

o Stability maintained within a range

• What are negative feedback, positive feedback and feed-forward systems? What roles do they  play in the body (give some examples of each)?

o Negative feedback is when the response is in the opposite direction of the stimulus ▪ It promotes stability and uses dynamic equilibrium

▪ Examples include

• Blood pressure

o Positive feedback promotes a change in one direction

▪ Promotes instability and disease

▪ Examples include

• Labor

• Blood clotting

• Fever

• Depolarization of a membrane to create action potentials

o Feed-forward is when your body anticipates and reacts to a change before it happens ▪ An example is digestion starts when you smell food

• What are the parts of a negative feedback loop?

o Set point

o Error Signal

o Effector

o Controlled Variable

o Sensor  

• Compare/contrast nervous system control vs. endocrine system control.

o Nervous System

▪ Short term

▪ Fast

▪ Uses neurotransmitters

▪ Irreversible

o Endocrine System

▪ Long term

▪ Slow

▪ Uses hormones

▪ Reversible

• What are the different functional parts of the nervous system?

o Sensory receptor, integrator, effector

o Organizaiton:

o Afferent (sensory) division

▪ Tactile, visual, auditory, olfactory, pressure, chemistry

o Integrative Division (usually CNS)

▪ Process information, creation of memory

o Efferent (motor) Division

▪ Respond to stimuli and direction from CNS

▪ Autonomic Nervous system

• Visceral response – organs, glands, smooth and cardiac muscle

• Parasympathetic – rest and digest

• Sympathetic – fight of flight

▪ Somatic Nervous System

• Skeletal muscle

• What is the difference between the parasympathetic and sympathetic systems? o Parasympathetic is when you are at rest and controls normal body function o Sympathetic is when you are under stress and only uses the necessary systems (ex:  stops digestion)

• Name the different neural circuits we covered in class and give an example of each. o Diverging circuit

▪ One neuron to many

▪ Motor neuron activating many muscle cells

o Converging Circuit

▪ Many neurons to one

▪ Rods in retina

• Many rods synapse to one cell, and many bipolar cells synapse with one  ganglion cell

o Serial processing

▪ One neuron to one neuron

▪ Cones in eye

o Recurrent or Reverberating Circuit

▪ kind of like a feedback mechanism

▪ learning and memory

o Lateral inhibition

▪ Activates one, inhibits others

▪ Allows for discernment of edges or points of sensory input

• What is the primary controller of the endocrine system?

o Hypothalamus

▪ Can be influenced by info coming rom the vertebral cortex or limbic system

• What are the different classes of hormones and how do they differ from one another in their  ability to be stored, travel in the bloodstream, interact with target cells and the type of  response from the target cell?

o Amino acid derived hormones

▪ Derived from tyrosine and tryptophan

▪ Tyrosine forms catecholamines like dopamine, norepinephrine, and epinephrine  and thyroid hormones like T3 and T4

▪ Tryptophan forms melatonin

o Lipid derived hormones

▪ Cholesterol can form a steroid backbone

• Gonadal (testosterone, progerterone), adrenal cortex, and placental  

steroids formed

▪ Arachidonic acid forms prostaglandins, leucotrines, and thromboxins but they  typically can’t act in endocrine function

o Peptide hormones

▪ Derived form DNA – RNA – Protein

▪ Peptides, proteins, and glycoproteins

o Steroid and thyroid hormones (lipid derived and some amino acid derived) hormones  are hydrophobic so they travel through the bloodstream with a hydrophilic transport  protein until they get to the target cell. Then they can pass through the plasma  membrane and bind to cytoplasmic receptors

▪ They cannot be made ahead of time and stored

o Catecholamines, melatonin, and peptide hormones are hydrophilic so they can travel as  free hormones in the bloodstream, but they can’t pass through the cell membrane so  they bind to a receptor and use a second messenger for signaling

▪ Can be made ahead of time and stored  

• What is unique about the production of peptide hormones?

o Peptides often aren’t produced in their final form

o Called a pre-propeptide

o The pre part of the pre-propeptide is a targeting signal for the Golgi and is cleaved  before the vesicle transport to the Golgi

o The propeptide goes through the Golgi and into a secretory vesicle where the pro part is  cleaved off. The pro part targets it for secretion and both are in the secretory vesicle o SNARE proteins are used in the secretion of the peptide

▪ SNARE protein attaches to the vesicle

• SNARE on the vesicle and tSNARES of the membrane and they attach

▪ Calcium influx into the cell drive exocytosis

o Example of this include insulin  and opiomelanocortin  

• What proteins are required for exocytosis of hormones from vesicles?

o SNARE and tSNAREs

• What hormones need second messengers?

o Hydrophobic hormones like steroid and thyroid hormones

• What are the different types of hormone interactions?

o Trophic

▪ Hormone functions to control secretion of another endocrine gland

• Regulatory hormones from hypothalamus to anterior pituitary  

o Synergistic

▪ Hormones work together and have a greater effect than one hormone

• Glucagon causes release of glucose stores. If epinephrine is present, you  get release of more glucose

o Permissive  

▪ One hormone enables action of a second hormone

• Secretion of epinephrine by adrenal medulla is partially dependent on  

release of cortisol

o Antagonistic

▪ One hormone produces an effect opposite of another hormone

• Insulin signals storage of glucose, glucagon causes release of glucose

• Define clearance with regard to hormones.

o The removal or inactivation of the hormone

o Clearance rate will determine the half life

o Some hormones have very short half life

▪ Few seconds to a few minutes

▪ Catecholamiens and peptide horomones

o Others have a long half-life

▪ Hours or days

▪ Steroid and thyroid hormones

• If they are bound to the hydrophilic carrier protein

• If free, they disappear very quickly

• What role does negative feedback play in hormone levels?

o All hormones fall under some kind of negative feedback control to regulate their  release.  

o The production of a hormone can often also be used to decrease the production of that  hormone

o Negative feedback combined with clearance determines how much is in the blood  • Know the basic HPA pathway (we will cover this more in the stress lecture 9/26). What is the  primary hormone known as the stress hormone?

o Happens during chronic stress

o Hypothalamus releases corticotropic releasing factor

o Stimulates pituitary to produce ACTH

o Adrenal cortex produces cortisol

o Will update after 9/20 lecture

Module 2: Memory and Learning – Review questions 

THE CEREBRAL CORTEX

• Where do we find the cerebral cortex?

o The dark, outside layer of the brain

• What three types of neurons are found there?  

o Granular Neurons

▪ Interneurons

▪ Some inhibitory, some excitatory

▪ Most found in sensory and motor cortexes

▪ Processing

o Pyramidal  

▪ Make up axon tracts, carrying sensory or motor information

▪ White matter (corpus callosum, tracts to/from spinal cord)

o Fusiform

▪ Make up axon tracts, carrying sensory or motor information

▪ White matter (corpus callosum, tracts to/from spinal cord)

• What is the reticular activating system? Where is it found? What is its function? o The RAS is responsible for constantly activating the cerebral cortex and is necessary for  survival

o It includes the reticular excitatory area, the mesencephalon, the hypothalamus, and the  thalamus

o It is responsible for wakefulness, arousal, consciousness, and attention

• If damaged what can it lead to? Malfunction of the RAS is thought to contribute to what? What types of drugs increase activity of the RAS? What type slow it down?

o If damaged, a person can experience sleep disorders, narcolepsy, Alzheimer’s and  senility (the late stage of Alzheimer’s), or coma

o Malfunction to the RAS can cause overactive or underactive RAS function

▪ People with an overactive RAS are hyperactive, talk too much, ad are very  

restless

▪ People with an underactive RAS could have ADD/ADHD, and their RAS can’t  keep up with sensory input

o Psychoactive drugs that increase RAS activity are Adderall, Cocaine, and Caffeine o Painkillers decrease RAS activity

• What two mechanisms are used to stimulate activity in the cerebral cortex? o Direct Stimulation

▪ Maintaining a background level of activity in wide areas of the brain

o Activation of neurohormonal systems

▪ Release facilatory or inhibitory hormone-like neurotransmitters to selected  areas of the brain

• What is the reticular excitatory area?

o Sends signals to the cerebral cortex and spinal chord  

o Signals down to the spinal cord

▪ Antigravity and postural muscle tone

▪ Spinal cord reflex activity

o Signals up to the cerebral cortex  

▪ Thalamus (where sensory info comes in)

• Rapidly transmitted signals and slow transmitted signals

o Activity levels determined by sensory input

o Positive feedback loop  

• Where do signals from the Reticular excitatory area go? What is the function of these signals?  Distinguish between the rapid signals and slow signals that go to the thalamus.  What  determines activity levels in the reticular excitatory area?

o Signals go down to the spinal chord

▪ Antigravity and postural muscle tone

▪ Spinal cord reflex activity

o Signals up to cerebral cortex

▪ Thalamus (sensory input)

• Rapidly transmitted signals

o Signaling lasts for a few milliseconds

o Release of acetylcholine

• Slow transmitted  

o Come from small neurons and small, slow axons

o Allows for a slow buildup of excitatory potential

• Inhibitory neurons release serotonin to decrease activity of the cerebral  cortex

• Rapid versus slow signals determined by sensory input

• What is neurohormonal control? What are the four systems found in the human brain – specifically what are the four hormones?  What is a basic function of each? o 3 pathways- hormones released for different functions

o Norephinephrine: excitatory to cortex

o Dopamine: inhibitory to basal ganglia

▪ Parkinson’s disease

o Serotonin: Inhibitory to diencephalon, cortex, and spinal cord

o Acetylcholine: excitatory to cortex, spinal cord

o Many other neurohonrmonal substances, including enkephains, GABA, glutamate,  epinephrine, histamine, endorphins  

• The major parts of the limbic system are the hypothalamus, hippocampus and amygdala.  What is the overall function of the limbic system?  

o The main function of the limbic system is to aid in learning and memory, as well as serve  a purpose in emotional response and behavior. It links other parts of the brain to the  cerebral cortex.

• The hypothalamus communicates with what parts of the brain? What are the functions of the  hypothalamus?

o Signals down

▪ Signals go to reticular areas

• Contributes to wakefulness and sleep

▪ Signals to autonomic nervous system

• Signal sympathetic or parasympathetic

o Signals Up

▪ To midbrain

▪ To cerebral cortex

▪ Associated with feeding behaviors and arousal responses

o Signals through the infundibulum

▪ To pituitary

• Releasing and inhibiting hormones

• What are the functions of the hippocampus?

o It is stimulated by sensory input and in turn distributes the information to the thalamus,  hypothalamus, and parts of the limbic system

▪ Signals go through the fornix

o Emotional response

▪ Plays a role in emotional responses such as rage, pleasure, etc.

o Plays a role in learning and memory

o Disorder of Hippocampus: Korsakoff’s syndrome

▪ Anterograde and retrograde amnesia

• Anterograde: can’t remember anything from before the damage  

occurred

▪ Retrograde

• Can’t form new memories, don’t remember anything new after the  

damage

▪ Caused by toxicity of alcohol or vitamin B deficiency

▪ Hippocampus and papaz circuit especially susceptible to damage

• What are the functions of the amygdala? If the amygdala is damaged or removed what  results?  

o Plays a role in processing olfactory sensory information in humans and lower animals o In humans, it plays a role in behavior not associated with olfactory stimuli o Receives sensory input from auditory and visual areas

o Sends information to the limbic system

o Take home function: notifies limbic system of body’s current status in relation to  surroundings and patterns behavior and thought response

o Kluver-Bucy Syndrome: loss of amygdala function

▪ Extreme curiosity

▪ Forget things rapidly

▪ Puts everything in mouth and swallow solid objects

▪ Extremely strong sex drive – try to mate with anything and everything

• Where are the primary reward and punishment centers in the brain? What role does reward  and punishment play in learning and memory?

o Reward centers are in the ventromedial nucleus and the lateral hypothalamic area in the  hypothalamus

o Punishment center found in the periventricular area in the hypothalamus o Reward and punishment are important in learning and memory because if there is no  reward or punishment associated with something, you won’t remember it  

▪ Habituation will occur without reward or punishment

• Continuous stimulation without reward or punishment

• Almost a complete lack of response by cerebral cortex

o With stimulation and a reward or punishment, there is a cortical response and a  memory is formed (typically long term memory)

• Define learning and memory. How are the two linked?

o Learning is the process that will modify subsequent behavior

o Memory is the ability to remember past experiences

o Memory is essential for learning because it serves as a record for the learning process o Learning also depends on memory because the knowledge stored provides a framework  to link new knowledge to  

• Describe the different types of memory.  How long do they last? (I don’t need specific times  just a generalization)

o Sensory Memory

▪ Develops from sensory information

▪ Lasts 1 milisecond to 1 second

o Short Term Memory or Working Memory

▪ If you pay attention to the sensory memory, it becomes a short term memory ▪ Lasts for about a minute

▪ Can only hold 7 things in your short term memory

o Long Term Memory

▪ Happens through encoding consolidation

▪ New synapses are formed

▪ Can last for days, months, years

▪ Memories that last for years are used often or are associated with a strong  emotion, reward, or punishment

▪ When you retrieve a long term memory, it is like a copy of it goes to short term  memory

• Describe the two types of long term memory and then the subcategories (more general for  the subcategories is fine).

o Explicit (Declarative) Memory

▪ Knowing what – being able to describe a fact or event

▪ Semantic Explicit Memory –facts

▪ Episodic Explicit Memory – events

▪ Associated with temporal lobe, hippocampus, entorhinal cortex

o Implicit (Non-declarative) Memory

▪ Knowing how to do something

▪ Procedural memory – skills and habits

▪ Classical Conditioning

• Skeletal musculature

• Emotional responses

▪ Priming

▪ Associated with cerebellum, and basal ganglia

• Define/describe what is meant by Encoding and Storage/Consolidation. What is important for  consolidation to be strong?

o Encoding

▪ Assigning a meaning to information to be learned

o Storage (consolidation)

▪ Converting short-term memory to a long term memory

▪ Rehearsal accelerated consolidation

▪ REM sleep helps consolidatoin

• What is retrieval? What is the difference between recall and recognition? o Retrieval

▪ Copying into short-term memory to use

o Recognition

▪ Only requires a decision as to whether you’ve seen the information before ▪ Activates only a few neurons

o Recall

▪ Actively restructuring all of the information from the memory

▪ Activates all the neurons

• Why is Henry Molaison’s story important? What was removed and what where the results?  What does that tell us about that part of the brain (be specific)

o He had uncontrollable seizures and a very low quality of life, so doctors removed his  hippocampus to stop seizures

o After the surgery, he couldn’t form new memories

▪ He lost explicit memory, but still had implicit memory

• Henry could learn to do new things that involved implicit memory, but  

he couldn’t remember that he knew how tot do them

o This was important because scientists were able to study what functions the  hippocampus really serve in creating and storing memories

• What are the Aplysia good lab models for studying memory formation? o Aplysia are good lab models for studying memory formation because they exhibit  explicit memory and we can use classical conditioning and can habituate them

o They can help us learn how other animals and humans form memories

• Define habituation? What happens at the neuron level during habituation? o Habituation is the decline in response due to repeated exposure to a stimulus o When habituation occurs, it is because less neurotransmitter are released at the  synapse

▪ It is not stored in memory because there is no reward or punishment associated  with it

• Define sensitization? What happens at the neuron level during sensitization? o Sensitization is when there is increased or amplified response to all stimuli o This occurs because more neurotransmitter is released at the neurons so there is a  larger response to a stimuli

• What did Eric Kandel and his colleagues learn from their work with Aplysia? Describe the basic  experiments that they ran and their findings. What is facilitation? Describe, in general, what  happened at the cellular level during facilitation.

o Through their work with Aplysia, Kandel was able to study habituation and sensitization,  and therefore short term memory

o First, they saw if they touched the siphon, the gill pulled in a certain amount ▪ If they continued to touch the siphon over and over again, the gill eventually  stopped retracting  

• Demonstrated habituation

o If they touched the siphon and then shocked the tail, the gill pulled all the way in ▪ If they shocked the tail multiple times in a row, and then just touched the  siphon, the gill reacted as if it had been shocked

• Demonstrated sensitization

• Memory of the shock can last for up to 3 weeks

▪ They saw that this happened because the sensory neuron in the tail synapses  with a facilitating neuron that then synapses with the motor neuron in 3  

axoaxonal synapses

• Leads to increased neurotransmitter release at the synapses

• What is long-term potentiation? What is the role of LTP in learning and memory? o Long Term Potentiation is the process of making new/more proteins and new synaptic  connections to form long term memories

o It is the process of release of glutamate and binding to AMPA and NMDA receptors. That  starts the process of forming new dendritic spines and synaptic connections  o Long term memories can’t be formed without long term potentiation

• Describe, in general, what happens at the cellular level during a normal synaptic transmission  and an LTP transmission. Why are they different? What role do the AMPA and NMDA  receptors play? What is the result of LTP physically? What ion is the most important in LTP?

o During a normal synaptic transmission, there is the release of glutamate from CA3,  glutamate binds to the  NMDA and AMPA receptors. There are low frequency action  potentials

▪ AMPA channel opens, sodium enters, and there is a small depolarization of CA1 o During LTP, there are high frequency action potentials

▪ Release of glutamate from CA3 happens, and more is released with increased  Action Potentials

▪ Glutamate binds AMPA and NMDA receptors

▪ AMPA opens and a larger amount of sodium enters, so there is a stronger  depolarization

▪ Magnesium moves out of the NMDA channel and sodium and large amounts of  calcium enter the cell

▪ Calcium binds to calmodulin and enzymes are activated through a second  messenger pathway

▪ The calcium/calmodulin complex travels to the nucleus to activate gene  

transcription and translation of proteins like CREB

▪ They also activate the formation of more NMDA and AMPA receptors that are  inserted into the dendrite membrane

▪ More dendritic spines are built to increase synaptic connections

o Normal synaptic transmission can create a sensory memory or short term memory o LTP creates a long term memory and alters the structure of the dendrites

o Calcium is the most important ion in LTP

• What factors influence memory formation and retention?

o Alertness, attentiveness, and concentration

o Interest, motivation, Need

o Mood, Emotion  

o Sensory stimuli

▪ Can increase memory function if it is linked to a sensory stimulus

Enteric nervous system and gut microbiota Review questions 

• What is the Gut-Brain or Brain-Gut Axis? What is its function?

o The Gut Brain is the enteric nervous system, which is the nervous system in your  digestive system

o It monitors and integrates gut functions

o It links emotional and cognitive parts of the digestive system

▪ Immune system

▪ Enteric reflexes

▪ Intestinal permeability

▪ Enteroendocrine signaling  

• What functions do the CNS and the enteric nervous system have in controlling digestive  function? How do their roles differ?  

o Enteric Nervous System

▪ Enteric nervous system controls the process of digestion completely

▪ Input from the CNS doesn’t alter process of digestion, but can alter when it  occurs

o CNS

▪ Sympathetic nervous system can stop digestion in a stress or fight or flight  response

▪ Parasympathetic nervous system can start the process of digestion through  salivation when thinking about or smelling food. This process is part of the CNS  because food hasn’t entered the digestive system yet.  

• What are the enteroendocrine cells? What do they produce (in general)?  o They are endocrine cells specialized for the enteric nervous system

o They produce GI hormones or peptides in response to stimuli

o They travel in the blood, diffuse as local messengers, or activate enteric nervous system  cells

o Examples of secretions include somatostatin, gastrin, CCK, insulin, glucagon, etc.  o Long reflex: gets CNS involved

▪ CNS activates myenteric plexus ???? stretch receptrs, chemoreceptors, peristalsis o Short reflex: just activates myenteric plexus, more localized

• There are many different types of neurons in the enteric nervous system (ENS from here on),  what are the ways they differ from one another?

o Motor neurons

▪ Control secretory cells

o Interneurons

▪ Activate muscle, secretory glands, enteroendocrine cells

o Sensory Neurons

• What are the two nerve plexuses that make up the ENS? Where are they located and what are  their functions?

o Myenteric Plexus

▪ Between longitudinal and circular muscle layers

▪ Control movement in the GI tract

• Muscle control in the gut wall

• Intensity and velocity of peristalsis (pushing stuff through)

• Inhibitory actions by neurotransmitters

o VIP (vasoactive intestinal polypeptide) inhibits sphincter  

contraction to allow passage of chime

o Submucosal Plexus  

▪ Monitor lumen

▪ Regulate blood flow

▪ Control secretory cell function

▪ Lines small and large intestines

• We went over three connections between the CNS and the Gut: Vagal, Thoracolumbar and  Pelvic. For the first two, what component of the Autonomic NS are they associated with. What

type of sensory and motor information would be carried in these axons (for all three  connections)?

o Vagal innervation is associated with the parasympathetic nervous system o Thoracolumbar innervation is associated with the sympathetic nervous system o Vagal

▪ Sensory/motor: esophagus, stomach, pancreas, small intestine, proximal end of  large intestines

▪ Sensory: lumen contents

• Indirect monitoring by chemoreceptors to detect nutrients and toxic  

substances

• Motor – same as myenteric plexus

o Thoracolumbar

• Digestion is controlled by long and short reflexes. What are the basic differences between the  two?

o Long reflex

▪ Gets the CNS involved

▪ CNS activates myenteric plexus ???? stretch receptors, chemoreceptors, peristalsis o Short reflex

▪ Just activates myenteric plexus

▪ More localized

• What are Hirschsprung’s and Chagas’ diseases? We compared these to CNS damage with  regard to digestive system function. Why are the CNS related damage not as bad as the ENS? o Hirschsprung’s Disease

▪ Distal ganglia of ENS fails to develop

▪ GI tract forms properly, but without innervation there is no way to empty bowel o Chagas’ disease

▪ Causes degeneration of ENS in colon, caused by infection of protozoon  

trypanosome cruzi via bite by kissing bug

o CNS malfunction has only a minor effect on digestion because the ENS is able to monitor  digestion by itself.  

▪ You can cut the vagus nerve and still have proper digestion  

• Now the gut microbiota….

• Composition in the GI tract is determined by what factors? What things can alter the  composition? Are everyone’s gut microbiota the same?

o Composition is determined by:

▪ Genetic factors

▪ Maternal health and well being

▪ Method of delivery

▪ Nutrition

▪ Maternal and postnatal exposure to antibiotics

o Composition can be altered by:

▪ Diet

▪ Pregnancy

▪ Transient microbiota through eating certain foods or taking probiotics

▪ Exposure to antibiotics

• Are we born with the adult composition of microbiota?

o No, microbiota diversity is small in newborns, it increases into adulthood, and decreases  again as we age.

• We can get transient bacteria (probiotics) from what types of foods?

o Foods that are fermented such as:

▪ Yogurt

▪ Pickles

▪ Kimchi

▪ Sourdough bread

▪ Sauerkraut

▪ Miso

• Based on studies in humans and germ free mice, what are the functions of the microbiota?  o Development of innate and adaptive immunity

o Modulate Gut motility, intestinal barrier, absorption of nutrients

o Influences stress reactivity and anxiety, regulate HPA set point

o Important for proper brain and ENS development?

• We focused on germ free mice – how are they germ-free? What types of abnormalities are  seen in these mice, associated with being germ-free (some of these may overlap with the  functions in the previous question)?

o Germ-free mice are delivered by C-section and taken into a sterile environment where  they are not exposed to microbes

o Germ free mice had different GI structure development

▪ Enlarged secum, metabolic structural differences, reduced intestinal surface  area

o They had a higher susceptibility to infection  

▪ Reduction in pyerspatch area – less immune tissue

▪ Less lymphocytes in overall immune system

o They had memory problems

o They had alterations in the concentrations of neurotransmitters such as serotonin  ▪ Serotonin is important in LTP, gut development, and ENS development  

• How do gut microbiota “communicate” with the CNS?

o Production, expression and turnover of neurotransmitters (i.e. serotonin, GABA) and  neurotrophic factors (BDMF)

o Protection of intestinal barrier and tight junction integrity

o Modulation of enteric sensory afferents

o Bacterial Metabolites

o Mucosal immune regulation

• What is the function of the intestinal barrier? Why have tight junctions? What happens when  the integrity of the barrier is reduced? What types of things cross into the body and what  happens as a result?

o We have outer and inner mucus layer to trap bacteria

o Epithelial cells are connected by tight junctions so nothing can leak through the  intestinal lining and into the blood

o Microbes maintain the tight junctions so that things don’t pass between the epithelial  cells

o Clostridium can break up the tight junctions ???? this causes diarrhea and food poisoning  symptoms  

o Stress can alter the tight junctions

o The leakiness of the epithelial cells when tight junctions are disrupted causes unwanted  materials to enter the blood stream

▪ Associated with celiac disease and IBS

o Bacterial metabolites can also cross into the body through nonfunctioning tight  junctions and interact with the CNS

• What are lipopolysaccharides? What are short-chain fatty acids? What effects are seen when  they leave the GI tract?

o Both are byproducts that are formed through bacterial metabolism

o Lipopolysaccharides  

▪ Release inflammatory cytokines  

▪ Inflammatory cytokine release can interact with the enteroendocrine cells and  stimulate the CNS and cause inflammation, activate immune system

▪ People with depression and chronic fatigue have high levels of antibodies to  lipopolysaccharides

o Short chain fatty acids

▪ Butynic acid, acetic acid

▪ Release stimulates the sympathetic nervous system

• Can lead to chronic stress

▪ Stimulates immune system/inflammation

▪ Can pass through the blood/brain battier and influence neurotransmitter  production in the brain  

• What cells make serontonin? We discussed serontonin when we did learning and  memory…what function does it have in that process?

o Serotonin is made in the cells of the myenteric plexus  

o It can also be made by streptococcus  

▪ Serotonin is important for LTP

▪ Serotonin is released at the axoaxonal synapses and helps with short term  memory

o Serotonin is used in axoaxonal synapses. It is released from the facilitating interneuron  and is necessary for habituation and sensitization. Those processes are required in order  to form memories.

• The gut microbiota may play roles in stress response, depression, cognitive abilities, and  behavior. Discuss the evidence we covered in class for each. This could be based on human  data, observations or in germ free mice. I don’t expect you to know the exact microbes that  cause or alleviate symptoms, just a general idea of what is known.

o Stress Response

▪ Gut microbes modulate normal stress response and activity of HPA

▪ Germ free mice have an exaggerated stress response

▪ If within the first 6 weeks of life, bifidobacterium is introduced in germ free  mice, the stress response becomes normal  

▪ Stress in early life in normal mice causes release of cortisol, activation of  

sympathetic and the stress response

• There were changes in microbe composition in these mice

o Depression

▪ The lipopolysaccharides and short chain fatty acids when released can lead to  depression

▪ People with depression and chronic fatigue have high levels of antibodies to  lipopolysaccharides

o Cognitive Abilities

▪ Germ free mice have memory problems

▪ They have alterations in concentrations of neurotransmitters such as serotonin • Serotonin is important in LTP

o Behavior

▪ Cirrhosis of the liver causes the liver to not be able to filter things like microbes  and microbe byproducts out of the blood

▪ People who have Hepatic Encephalopathy experience personality changes, but  when treated with antibiotics, their personality returns to normal even though  they don’t have an infection

▪ If microbes were taken from adventurous mice and put into shy mice, they shy  mice became adventurous  

Stress Review Questions 

• What is the HPA axis? What does it control? What are the three structures that make up the  axis?

o Hypothalamic pituitary adrenal axis

o It controls the endocrine side of stress response and the overall release of cortisol  through production of CRH and ACTH

o Hypothalamus, anterior pituitary, and adrenal cortex make up the axis

• What hormones are produced during a stress response? Which glands secrete them and what  do they do?

o The hypothalamus produces CRH (corticotrophin releasing hormone)

o It then travels to the Anterior Pituitary were it signals for the production of ACTH  (adrenocorticotrophic hormone) by the anterior pituitary

o ACTH travels to the Adrenal cortex where it signals for the production of cortisol by the  adrenal cortex

• How are levels regulated?

o Levels are regulated through a negative feedback loop

o Cortisol and ACTH provide negative feedback to the anterior pituitary and hypothalamus  to prevent the production of more CRH and ACTH

• What other hormone is released during a stress response? What role does it play? o Vasopressin, or antidiuretic hormone is also released

o It goes to the posterior pituitary and makes sure you can respond to other novel  stressors

▪ If you are stressed about a test and the building catches on fire, it makes sure  you can respond to the new stress of the building on fire

• Immediate alarm response is mediated by what system? Neurotransmitter? What are some of  the effects?

o Mediated by sympathetic nervous system

o Epinephrine is the neurotransmitter

o Effects include increased heart rate, increased ventilation, increased vasoconstriction of  specific regions such as skin, decreased digestion, increased glucagon activity to break  down glucose, increased fat catabolism, and decreased insulin production to stop  storing glucose

• The later or continued response is mediated by what system? What hormones? What are the  effects?

o Driven by the HPA axis

o CRH, ACTH, and cortisol are produced

o The actions of insulin are opposed, liver gluconeogenesis increased, muscle/bone  protein catabolism increases, Thyroid stimulating hormone, gonadotropins, and growth hormones are inhibited, fat is catabolized to free fatty acids and glycerol

• Cushing syndrome patients suffer from what? How does this help us understand chronic  stress?

• How does cortisol affect the ENS and what is the gut reaction to stress? o Cortisol inhibits digestion and activity of the ENS

o The ENS also has receptors for cortisol that when activated through binding, contributes  to stress response by the gut

• What does PGE2 do? What does this tell us about the immune system and stress response? o PGE2 is released by immune cells and it stimulates the zona fasciculata to produce more  cortisol

o This tells us that the immune system increases stress response

• What do the studies on germ-free mice tell us about development of the HPA axis and gut  microbiota?

o Germ free mice have an exaggerated stress response

o However, if bifidobacterium are introduced within the first 6 weeks of life, stress  response is corrected and normal

o This suggests that the gut microbiota help with the development of a normal  functioning HPA axis, and the development is time sensitive – developed within first 6  weeks of life  

• How does the limbic system influence stress response?  What functions do the hippocampus  and amygdala play in HPA activity?

o Most structures in the limbic system connect to the hypothalamus and effect  sympathetic output and HPA axis function  

o The have receptors to cortisol and can either inhibit or enhance stress response o The hippocampus will terminate HPA response to stress

▪ If hippocampus is activated by binding cortisol, it inhibits cortisol secretion o The Amygdala will activate the HPA axis and promote cortisol secretion if it is activated • What effect does chronic stress have on the hippocampus? Learning and memory? o Chronic stress can damage the hippocampus because of the high cortisol levels  o They can shrink the hippocampus and damage it  

o If the hippocampus is damaged, it hurts learning and memory formation because the  hippocampus is essential in forming long term memories  

Recitation 

• Resting Membrane Potential

o Need a concentration gradient

o Need a selectively permeable membrane

o Need a mechanism to maintain the concentration gradient

o Na+ is high in ECF

o K+ is high in ICF

o Cl- is high in ECF

▪ Don’t see a lot of movement in because the negatives in the cell are up against  the membrane, so if Cl- tries to go in, it is repelled

• Types of channels

o Resting (Leak) channels

▪ Always open

▪ We have many K+ leak channels, but few Na+ leak channels

o Voltage Gated Chanel

▪ Opens in response to change in the membrane potential

o Ligand gated channel

▪ Opens in response to a specific extracellular neurotransmitter

• We maintain concentration through active transport with the Sodium/Potassium ATPase pump. o 3Na, 2K, 1ATP

• Membrane Potential

o Charge difference across the membrane

• Action Potential

o All axons aren’t the same – they may have different thresholds

o Action potentials are all or none events that have the same amplitude for all stimuli,  weak or strong

o Frequency of Aps is quantitative data

▪ Always giving off constant signals for things like blood pressure – a change in  frequency of Aps causes a response

o At resting membrane potential, voltage gated sodium and potassium channels are  closed and leak channels are open

o At threshold, voltage gated sodium channels opens and sodium flows into the cell  rapidly. Potassium also opens, but it opens very slowly

o At the peak of depolarization, sodium channels close and potassium channels are open  all the way

o As the cell gets close to threshold again, the potassium channel starts to close, but  closes very slowly so the cell gets slightly hyperpolarized

o At -40 mV the sodium channel resets

• Refractory period  

o During the absolute refractory period, you cannot stimulate another action potential no  matter how strong the stimulus

▪ Voltage gated sodium channels are already open or inactivated

o During the relative refractory period, you can stimulate an action potential but you need  a stronger than normal stimulus

▪ During this period, there is a lot of K+ leaving the cell, so it takes a lot of Na+ to  overcome and bring the cell to threshold

• Conduction

o Conduction of current through a neuron occurs in 2 ways:

▪ Active regenerative conduction

• No decrement of signal

• Axons  

• Action potential

▪ Passive electronic conduction

• Depends on the physical properties of the cell

• Conduction degrades with time and distance

• Dendrites, soma, and some axons

• Local potential

• Unmyelinated regenerative conduction

o Each segment of the axon must depolarize and generate an AP

• Myelinated regenerative conduction

o Only have to depolarize the are in between the myelination

o As the sodium comes in you have to make sure enough diffuses down the axon to  depolarize the next area, so myelination cant be too far apart

• Cable properties of neurons

o Membrane resistance and internal resistance determine the length constant of the  membrane

o The length constant is the distance over which a membrane potential will drop by 63% o Myelinated axon = high Rm

o Large diameter = low Ri

• Types of synapses

o Axodendritic

▪ Axon to dendrite

o Axosomatic

▪ Axon to soma

o Axoaxonic

▪ Axon to axon

• Action potential

o Membrane of soma depolarized

o Voltage gated Ca2+ channels open

o Synaptic vesicles go to docking protein SNARE

o Neurotransmitter released and binds to receptor on neighboring neuron o Can have EPSP depending on what channel it binds to

▪ Excitatory

▪ Depolarizes membrane – local potential

▪ Sodium channels open

▪ Length constant determines signal

o Can have IPSP

▪ Inhibitory

▪ Hyperpolarizes membrane

▪ K+ or Cl- channels open

• Active zone

o Are on postsynaptic knob where vesicles bind to docking protein  

• For neuromuscular junction, it is always Ach released, it is always excitatory, and we always  reach threshold and send and AP

o If we didn’t want the muscle to contract, there would be no signal sent at all • General characteristics  

o One way conduction

o Allows signals to be directed toward specific targets

o Over 40 substances identified as neurotransmitter

o Altered by amount of neurotransmitter available, pH of ECF, Ca2+ in ECF, and drugs o Neurotransmitters can be excitatory, inhibitory, or both depending on the channel they  bind

• How to get rid of neurotransmitter in synaptic cleft after AP stops

o Some are taken back up through channel to be repackaged and reused

o GABA can use reuptake, or it can be take up by an astrocyte, uses an enzyme to change  it to glutamate, the another enzyme to change it to glutamine, then brought back into  cell where it is turned back to GABA

o Ach is broken into choline and acetate. Acetate is processed out and choline is taken  back up where it combines with a new acetate from mitochondria, is repackaged as Ach  to be used again

• Synaptic Fatigue

o Happens when synapses are repetitively stimulated at a rapid rate until  neurotransmitter stores are depleted

• Long term facilitation

o Enhanced responsiveness following repetitive stimulation

o Mechanism is a build up of Ca2+ ions in the presynaptic terminals  

▪ Causes more vesicular release of neurotransmitter

• Long term depression

o Reduced responsiveness following low frequency stimulation

o AMPA receptors removed from post synaptic cell

o Used in learning and memory

o Allows you to trim the network to make it more efficient  

o Without this you would run out of space for more dendritic spines to form new  memories

o Low frequency stimulation

o Glutamate binds receptors, sodium depolarizes membrane, calcium comes in o Instead of activating kinases, protein phosphatases are activated to inhibit enzymes in  pathway

o Can happen during LTP

• Temporal and spatial summation

o Temporal (time)

▪ When a second AP comes in before the sodium has left form the 1st AP, you can  sum them together to cause a stronger depolarization to reach threshold

o Spatial (space)

▪ Aps from two different synapses can be summed together to create a strong  enough depolarization to reach threshold

• Drug Effects

o Agonistic

▪ Enhance synaptic activity

▪ Make more neurotransmitter

▪ Enhance release of neurotransmitter (more) ▪ Drug binds to postsynaptic receptor

o Antagonistic

▪ Block synthesis of neurotransmitter

▪ Block release of neurotransmitter

▪ Block postsynaptic receptor

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