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VANDY / Neuroscience / NSC 2201 / What do you call the signal movement towards the inflammation site?

What do you call the signal movement towards the inflammation site?

What do you call the signal movement towards the inflammation site?


School: Vanderbilt University
Department: Neuroscience
Course: Neuroscience
Professor: Leslie smith
Term: Spring 2017
Tags: neuroscience, neurobiology, brain, Psychology, conditioning, learning, memory, Systems, disease, disorders, treatment, habituation, Sensitization, stress, depression, ocular, dominance, stem, and cells
Cost: 50
Name: Exam #4 Focused Concepts and Key Terms
Description: These notes cover exam-likely material.
Uploaded: 04/23/2017
14 Pages 54 Views 4 Unlocks


What do you call the signal movement towards inflammation site?

The future: Make stem cells from your own cells

to implant


HRP = Horse Raddish Peroxidase = retrograde axones marker,

non -

Aguayo never showed successful connection to the brain (functional)

What are some examples of delusion?

Neural inflammatory agents cause chromatolytic cells and depression "Genes set the risk, environment pushes one over into disease We also discuss several other topics like What is the difference between basic ethics and applied ethics?

"Mental illness is any behavoir out of self control and not in ones best interest If you want to learn more check out What's an example of positive economics?

- Particularily in the cerebral cortex

How is protein kinase a activated?

Don't forget about the age old question of How were funds allocated during the government spending in 2014?
If you want to learn more check out Which school of thought believes that every trait has a purpose?
Don't forget about the age old question of Who founded the three laws of motion?

Cortisol causes sympathetic activation (NE Norepinephrine)

The hippocampus has the most glucocorticoid receptors. If an antibody to glucocorticoid receptors is injectedthe hippocampuses can be visualized SSRI (5-HT) antidepressants like Prozac and 2010ft depress libido Cytokinesi signal movement towards inflammation site (immune Avolition: severe lack of initiative and motivation Delusions: Implausible beliefs, thought insertion Schizophrenia Experience and stress starts at conception, invitre. like birthing We also discuss several other topics like What pertains to the metabolic rate of an animal while it is out in the field?

Male Female - Oxygen/circulation, trauma.

ud Soups



20 years

Males show/present schizophrenia


20 years


40 years



Sam LIP - Long-Term potentiation as a model for synaptic plasticity: Teretan_ Induced by brief tetanus (electrical shock, high frequency for less then I séle

•LIP sticks around for weeks, tomaty months... which helps our memory

• Temporal and spatial surmation of Epsp's (cooperativity) strengthens Requirement for LTP: Synapse must be active when the post synaptic

element is strongly depolarized










Low frequentemente

LTD is just the opposite :le

The low frequency stimulation is not enough to activate the post synaptic neuron, so the Synapse is weakened, or destroyed

Action Potential

ha Before Forgetting After Forgetting S

p re synaptic aron A Voltage recorder

EPSP in post synaptic


plenty of cart

• very flat

entry post-synaptically sub-threshold. Catt ☆ Note: Synapses stay intact in the abscence of stimulation, it's just

when there is sub-threshold stimulation that they brook down.


mi ved

Learning; "when the same AP Causes a larger post synaptic effect


The Wisconsin Card Sorting Tests Wercking alleroy and Pro - frontal cortex. Reconsolidations when we recall a memory it becomes suceptible to permanent






To treat Neuroleptics, sjeze and block the D2 receptor

☆ NEW Ocular Dominance: Monocular deprivation for

I one eye for 2 years Normal person's tangential sections I starting at 2 weeks of age through layer IV of Striate cortex shows expanded ocular shows equal width Stripes for LGN I dominance columns of the of both eyes. W

non deprived eyes




-Ocular dominance Columas expand/ for nod-deprived - the vertical white space is increased!


Memory Functions of the hippocampal sal system Summary

D) Hippocampus gets information fróm grid cells (where) 27 Combines it with information from sensory input (what).

3) = What happened and where it happened 4) A DECLARATIVE MEMORY!!!

For a neuron: The difference between no input and weak input is the

amount of NMDA receptors activated

Protein kinase A (PKA) is activated by CAMP, phosphorylation of potassium channels makes them close to plant so repolarization happens slower. Salient Event: Getting Vandy Acceptance letter - Involves a structural brain change

that will "Make a Memory" for life time


Thanks to everyone who has studied with my notes.




Healing Broken Brainsi

Embryonic Cortex of thy - and thy-d mice transplanted into adult host cortex can help boost NT levels.

Neuronal stem cells:

- Available 6 days after conception from Blastocyst.

- Can beal spinal cord injury Also injecting substances to block "nogo" receptors promotes growth - after spinal cond injury

Regrowth by Axon Type: en

o The closer the cut

is to the cell body, the more likely the neuron

will die. t (sprouting only) modulatory LCNS OF e Telongation only sy (farmer with arms cat off

regained feeling after re-attachment: ONS -

- True Regeneration


*CNS specific synapes cannot regenerate exactly like they broke

because there are no membrané markers. Memories, skills, etc. Will I always be impaired even if Aguayo's regeneration method works.

- t put schwann cells inte spine losion stem cell tissue can help set "brain tone" in modulatory CNS systems by boosting DA and Ach

levels which improves cognitive activity. Develeped neurons don't work because they die when dendrites are ripped during transplant

Neurons grow along fibronexin and can be "fertilized with growth factors. - transection of spinal cord can recover to 30%




Habituation. Molecular Mochanism: Cast channels in sensory

neuron open less often, lower presynaptic calcium concentration resuts in less and less heuro transmitter release.

12-29 Axon Terminal

sensitization Molecular Mechanismi (e

5-HT is released presynaptically by 229 onto sensory / FG-protein coupled receptor is activated by 5-HT"

- Activating of Adenyl Cyclasé y Production of Amp from AMP

→ Activating protein kinase A Adenylyn 572 I phosphorylation of kt channels closes cyclam

decreased it conductance prolongs the Ale them!

More Cat entry CAMP Am sprotein - More NT release per AP

Protein kinase A - Gill withrawl reflex is restored active)" proteine



sensory neuron


axon terminal



AMPA - ligand-gated receptor that conducts Na" (lets voltage set to Nova activation) NMDA = Ligand and voltage gated, Conducts Nat and cast Bear Model: Calcium non ha concentration : apoptosis (me an tha).

<l mismo mar USC o latt levels too low: long-term cell depression caused by phosphatases I Low Frequency stimulation which close Catt channels quicker (by removing)

ogh ny ton too high = long-term potentiation caused by kinases

which phosphorylates the potassium channel Conditioning changes Invertebrates: Presynaptic Vertebrates: Post Synaptic



100 high

Induce LTP by High


I frequetimulan


EXAM U - Dementia/Alzheimer's FAMILTAL_ Alzheimer's Disease I

patein E Sporapie Alzheimer's Disease Are gene over expression> Arabian Apos, head injurys Aging over production of famyloid avst

Inadequate ß-amyloid clearance

deposition of ß amyloid plaques

Inflammatory response, release of cytokines Deurite injury due to toxic ß-amyloid plaque levels _ disruption of ionic homeostasis and metabolism: Oxidative stress

Altered kinase phosphatase activity = hyperphosphorylated tau

neurons die Neurotransmitter levels drop tan becomes tangled in plaques.

Regeneration : _

-- Begrowth and reformation of synapse

- Only Only possible in Peripheral Nervous System PNS - Put PNS schwang cells in the CNS and some regrowth happens."

Chromatolytic: "Sick Neuron"

(chance of healing)


- learned adjustment of behavior - Adjustment in synaptic strength of remaining Axons


EXAM #4 Classical Conditioning:

Conditioned Strong tail shock Lunconditioned stimulus) + Stimulation of siphon (Stimulus = greater activation of adenyl cyclasé than only I alone, since is

increases cada current in presynaptic celle

Higher [code] increases adenylyl cyclase sensitivity to G-protein.

- activation Learning : I Presynaptic Ca2+ pulse coincides with adenyl cyclase activation by G - Protein High cAMP concentration → High protein kinase

activity More Neuro Transmitter

Conditioning Both sensitization and

Sensitization is

Classical: latt Classical conditioning use

is a product of) I and serotonin i protein kinase

Serotonin only act at the samel


Seratonin activation causes potassium channels

to flow. (Activated by noxious' stimulus.)


Working Memory vs. Short Term Memory

- Seconds

- Minutes / hours/ -ex: Given a phrase to repeat

- Forgettable without reading it each time Structural changes to the synapse over time :(


Postsynaptic Changes increase in number of axon terminals -phosphorylation of AMPA receptors -larger terminal size

- Addition of new AMPA and NMDA receptors - More neurotransmitter release - Post Syrapse element size increase

Morris Water


proves Hippocampus is necessary for Spatial memory. When the NMDA receptors are blocked the mouse forgets where the underwater platform is."

Study So


☆ stress





EXAM #4 Major

depression Depression: Melancholia vs. Atypical

- Fatique, lots of sleep - Weight loss

- Hyperphagia' weight gain Hea exis: ICRH 9 ACTH! - Variable hedonic response L a ↑ cortisol

4 molt Variable mood – Anergiallow energy) _ variable motivation Predispositions Stress, Genetics, Childhood abuse

"Push-Pull regulation of the hippo tempes. HPA axis

by the amygdala and hippocampus Chippocampus

Samygdalas s Hypothalamus



increased cortisol release Diathesis-Stress Model of melancholia: Antidepressants:


increased 5-HT and NE

APA axis disregulation

GRS PKA - Melancholia)

Neuron division

Neuron growth Excess Cytokines cause inflammation

decreased cortisol and depression ceases


Brain-derived neurotrophic - factor



I Lecture

EXAM #4 The brain is vulnerable to disease; -ne cell division

_ -Specialized tissue areas

- unique blood supply I Concussion Molecular Mechanism: -Tight Spare (skull

” Stretch and shearing of axonal membranes

kt is allowed to rush out, as potential approaches zero consciousness b blood supply is reduced to -50% - Glue is released from depolarized or dying neurons

+ Over-activation of NMDA receptors' by Glu

→ Increased Catt influx causes excité toxicity Stroke: Occlusive Hemorrhagic

embolism/ thrombus aneurysm / AVM AL Blockage Mo Infarct Neurons:





Ischemia: - Damaged neurons

Had Cancerous Brain Tumor: Astrocytomas - Brain Tumor - LED KENNEDY low-grade: 5yrs to death Anaplastic astrocytoma : 104 live 5 years

(GBM: Ted kennedy died within Il months

Brain Tumors resist treatmenti

- Blood Brain Barrier - tumor cells migrate through the brain - Hard to tell the difference in tissue


Healthy/ tumor

El cooperativity

compour,ds to improve learning

Exam #4

key Terms Non - Associative Learning:

- Change in behavioral response

that occurs with stimulus repitition

☆ Procedural memory is easier to study

memories have an ethereal quality about

because declarative them

Instrumental conditioning

- Learning to associate a motor response with a Meaningful stimulus


Memory Consolidations

short-term memory + sensory information


Long Term Memory

☆ Dissociated amnesia does not cause other cognitive defects

Retrograde amnesia:

often resulting from brain trauma, forget prior events. X Memories are widely distributed, but some areas hold more

Hebbs definition of Cell assembly: Neurons simultaneously activated by an external stimulus that are reciprocally interconnectado Temporal lobe structures for declarative memory consolidation

- Hippocampus - Fornix - Parahippocampal and rhinal cortical areas

Striatum = Procedural memory


EXAM #4 Schizophrenia:

- positive symptoms: delusions, hallucinations, catatonic - - negative symptoms: reduced emotion _ behandan

poverty of speech, avolition, pour memory - caused by mass' activation of dopamine receptors Anxiolytic drug dasses:


+ Serotonin-selective reuptake inhibitors Antidepressive drugs

Linhibit reuptake of released serotonin and morepinephrine

LA drug that blocked dopamine receptors:

- Classified as a neuroleptic - used to treat schizophrenia

- causes parkinson's like symptomse Agoraphobia: Anxiety about the difficulty of escaping


- Acute precipitating W Schizophrenia: 1-genetika

Youth Weinberger Dopamine Hypothesisi iCoyle Glutamate Hypothesis - Meso-Cortical ba pathway impaired so DA__ more glutamate improves symptoms

brainstem neurons don't stimulate the pre. frontal #- Glu dysregulation may occur in

cortex well enough (negative symptoms). The regional subpopulations of sz brains.

prefrontal cortex can't appropriately inhibit - Enhancing Glu transmission DA brainstem neurons from over stimulating through the NMDA receptor heals

limbic areas (no accumbens) which leads - Sub-sensitivity of NMDA receptor to the positive symptoms i

i which is activated by Glutamate




a mal nutrition

-selective cell

decth -less my etch

El decreased



- anoxia


Study SODA


EXAM #4 Deafferentiation:

T Cutting afferent axon

3 resuts in axonal elongation synapse formation,

Collateral Sprouting _ steps to enhance specific fiber growth into and around embryonic transplant tissues

- Electrically stimulate transplant cells to increase Sout their activity levels

- prevent Modulatory fiber ingrowth - Identify trophic substances that would enhance

specific fiber growth in adult brains - Alzheimer's Cure:

Fransplant embryonic presen ophola

septal cholinergic neurons into adult hippe campus True regeneration: - -Sprouting

- Axonalelongation

-Synapse formation CNS Pathways able to regenerate:

-- Monoaminergic projections

- Cholinergic projections TENS Modulatory fiber system can have

Laxonal Blongatione (ins_specife fiber system conot)


in a



can grow, if only they are placed environment? Can we mimic the environment?

(Future Research Area)


EXAM 4 NMVA receptors "coincidence detectors"

-Ton movement through the channel requires binding of

glutamate to the NMDA receptor plus depolarization of the postsynaptic membrane

Panic disorder

Frequent panic attacks consisting of discrete periods of sudden, intense fear fulness.

stress Besponse:

- sympathetic nervous system activation - avoidance behavinir - release of cortisol from adrenal glands - increased arousal

_ Cortisoli

- hippocampal cell death -Changes in growth factors -changes in glucocorticoid receptors in the hippocampus pothalamic-pituitary-adrenal axis

mediates the humeral (blood fluid) part of

the stress response Hippocampus regulation of of HPA axis: o

-detects cortisol levels and inhibits Crtl release.

(cortico tropin releasing hormone is from the byps thalamus) When Adrenal gland spikes cortisol - fight or flight Bipolar Disorder

Mania & Depression

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