New User Special Price Expires in

Let's log you in.

Sign in with Facebook


Don't have a StudySoup account? Create one here!


Create a StudySoup account

Be part of our community, it's free to join!

Sign up with Facebook


Create your account
By creating an account you agree to StudySoup's terms and conditions and privacy policy

Already have a StudySoup account? Login here

Midterm two studyguide

by: ask0429

Midterm two studyguide NEUROSC 3000 - 010

GPA 3.6

Preview These Notes for FREE

Get a free preview of these Notes, just enter your email below.

Unlock Preview
Unlock Preview

Preview these materials now for free

Why put in your email? Get access to more of this material and other relevant free materials for your school

View Preview

About this Document

These cover ch. 6-7 and part of ch. 23 which will be on the exam
Introduction to Neuroscience
Robert Boyd
Study Guide
50 ?




Popular in Introduction to Neuroscience

Popular in Neuroscience

This 7 page Study Guide was uploaded by ask0429 on Sunday March 20, 2016. The Study Guide belongs to NEUROSC 3000 - 010 at Ohio State University taught by Robert Boyd in Fall 2015. Since its upload, it has received 20 views. For similar materials see Introduction to Neuroscience in Neuroscience at Ohio State University.

Similar to NEUROSC 3000 - 010 at OSU

Popular in Neuroscience


Reviews for Midterm two studyguide


Report this Material


What is Karma?


Karma is the currency of StudySoup.

You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!

Date Created: 03/20/16
Neuro 3000 Midterm 2 Study Guide Neurotransmitters and Receptors (CH. 6)  Intro and History 1  transmitter found = ACh (acetylcholine) [Loewi and the vagus nerve experiment]  Cell that produce/release ACh = cholinergic [coined by Dale] *similarly: Norepinephrine (NE) = noradrenergic        GABA = GABAergic        Glutamate (Glu) = glutamatergic        Peptides = peptidergic    ACh + molecular machinery = cholinergic system [same naming device for all neurotransmitter  system]  Classification of neurotransmitter:  1. Molecule synthesized/stored in presynaptic cell 2. Released by presynaptic terminal in response to stimulus  3. Must produce response in postsynaptic cell both in vivo and experimentally (same  response)  If all 3 criteria are met through experimentation, then the candidate becomes a neurotransmitter Methods of study:  1. Immunocytochemistry: viewing localization of specific molecules. Make antibodies to  specific transmitters or enzymes which synthesis the transmitter. Antibodies mark the  cells that use transmitter or cells that have enzymes that make transmitter  2. In situ hybridization: localization specific mRNA transcripts for proteins. Detect RNA  expression using specific probe labeled with radioactivity, colored, or fluorescence  product. Probe = complementary mRNA strand. i.e. FISH: brightly colored fluorescent  molecules attached to probe view directly under appropriate microscope  Studying transmitter release {difficult to do hardest condition to satisfy}  1. Test fluid from near axons/cells for substances after stimulation [Loewi and Dale] Works  in PNS, not so much in CNS (intermingling of various synapses using different  transmitters can’t stimulate single population of synapses using traditional methods)  2. In vitro slice: stimulate alive brain slices [bathed in K+ and Ca+2 solution] and test what  is released  3. Optogenetics: activates 1 specific type of synapse at a time  a. Induce 1 population of neurons to be light sensitive [stimulated by flash of light that  doesn’t affect other surrounding neurons] Transmitter releases has to come from light  sensitive synapses *can’t be sure molecules collected were releases by pre or post  synaptic termination [could be released by secondary consequences of synaptic  activation  b. Applied experimentally to produce same response as in vivo  i. Microiontophoresis: thin glass pipet, filled with ionized solution, positioned  nest to postsynaptic membrane and release transmitter by passing currents  through pipet or pulse of high pressure. Microelectrode measures effect.  ii. Studying receptors [ACh, GABA]: 2 different neurotransmitters can’t bind to  the same receptors [ACh]. Each transmitter can bind to different subtypes Neuropharmacology analysis 1. Agonist and antagonist used  to classify receptor subtypes i.e. Nicotine: agonist in skeletal muscles, no effect in receptors of the heart      Muscarine: agonist in heart, no effect in skeletal muscle  2. Selective antagonists i.e. curare inhibits Nicotinic receptors [paralysis]        atropine: antagonizes ACh @ muscarinic receptors [pupil dilation drops]  3. Drugs: mediate synaptic excitation in CNS i.e. NMDA, AMPA, Kainate receptors for Glu       NE: alpha, beta receptors        GABA: A and B receptors  Ligand Binding Method 1. Use labeled ligands to bind specifically to receptors  *Ligand: neurotransmitter, agonist, antagonist, toxins, and components of venom.  Radioactive or nonradioactive label Molecular Analysis  1. Cloning of many receptors cDNA’s  2. Protein sequencing 3. Diversity of subtypes larger than expected from binding and pharmacology Neurotransmitter Chemistry Most transmitters are amino acids: amines made from amino acids or peptides Dale’s principle: neuron has only one transmitter [Exceptions: peptide containing neurons violate principle dual transmitter neurons known (co­transmitters)]  Cholinergic Neurons 1. Neuromuscular junction made by all motor neurons in spinal cord and brain  2. 2 major groups of cholinergic neurons in the brain  a. Basal forebrain: learning, memory (Alzheimer’s effects these systems)  b. Dorsolateral pontine tegmental constellation: excitability of sensory relay system 3. Also used by many circuits in autonomic neurons system 4. ChAT [manufactured in soma and transported to axon terminal] is a marker of  cholinergic cells as it synthesizes ACh in cytosol of axon terminal  5. Choline (rate limiting step) + Acetyl CoA =(via ChAT) ACh( via ACh transporter  high vesicular H+) Vesicle(release) extracellular fluid and receptors(via AChE  [acetylcholinesterase for degradation]) Choline (taken back into cell) + Acetic acid Catecholaminergic Neurons 1. Tyrosine = precursor for catecholamine class neurotransmitters [Dopamine (DA), NE,  epinephrine(Epi){function in CNS unknown}], good marker for catecholaminergic  neurons 2. Regulate movement, mood, attention, and visceral function 3. TyrosineVia TH(rate limiting step) Dopa Via Dopa decarboxylase   DA Via DBH   NE Via PMNT  Epi 4. End product inhibition: decreasing release of transmitter = inhibition of TH = decreased  production of transmitter, increasing Ca+2 (increasing release) = increase TH activity 5. DBH found in vesicle NE made in vesicle [locus coerules]  6. PMNT found in cytosol of adrenergic axon terminal NE synthesized, released, PMNT  synthesized, then Epi formed then packed into vesicle 7. Epi is hormone when released by adrenal gland into bloodstream  8. Transporter(high membrane Na+) for selective reuptake [reuptake or  degradationenzymatically destroyed using MAO a. Blocked by amphetamines and cocaine Serotonergic Neurons [few in number, widespread from raphe nuclei, used in pain signaling]  1. Serotonin (5­HT): role in mood, sleep, emotional behavior regulation, precursor to  melatonin in pineal gland 2. Tryptophan (rate limiting)via tryptophan hydroxylase 5­HTP via 5­HTP  decarboxylase 5­HT  3. Serotonin reuptake (SERT) high Na+  a. Blocked by SSRI’s, ecstasy [long term use destroys serotonergic projections]  b. Either reuptaken or destroyed by MAO Amino Acidergic neurons  1. Glu (major excitatory neurotransmitter) [learning, memory, motor functions,  development, plasticity, implicated in ALS, can cause excitotoxicity(stroke) LTD/LTP],  Glycine (Gly) [Glu and Gly synthesized by glucose], and GABA (main inhibitory  neurotransmitter) [unique to neurons that use it as a neurotransmitter]  2. Transporter: concentrate Glu in vesicle until 50 mM 3. Glu GAD [good marker] GABA 4. Loaded into vesicles by specific transporters  5. Na+ dependent transporter selective reuptake into presynaptic terminal and glia 6. GABA: A receptor [Cl­ gated channels] B receptor [G­protein­coupled receptor], present  in local circuits interneurons and purkinje cells, not present in peripheral tissue and  nerves, barbituates modulate GABA receptors [used to treat epilepsy], signaling deficits  = Huntington’s, Parkinson’s, Schizophrenia, senile dementia, VIAAT (transporter),  removed by GAT, broken down in mitochondria, B6 is synthesis cofactor 7. Glycine: half of inhibitory synapse in spinal cord, synthesized by serine, VIAAT  transporter, removed by plasma membrane gly transporter Other Neurotransmitters 1. ATP: opens cation channels in sensory and autonomic ganglia and motor neurons,  nucleotide receptor, binds to purinergic receptors(ion channel and G protein), degraded  by extracellular enzymes  2. Endocannabinoids: retrograde signaling, not in vesicles, membrane permeable, bind to  CB1 receptors, inhibit presynaptic Ca+2 channels 3. Peptide neurotransmitter: 100+, processed like proteins, endorphins, enkephalines,  dynorphia, substance P, can be in 1 or more vesicle, often co­released with small  molecule transmitter, G­protein coupled receptors,  4. NO: comes from arginine, released by some post­synaptic neurons, retrograde signaling,  permeable 5. CO: messenger  Transmitter gated channels Model is nicotinic AChR from skeletal muscle with 5 subunits (4 types α, β, γ, δ): ACh  binding sites require alpha subunits,  ACh bound opens the channel.  Each subunit type has unique sequence that’s very similar, 4 hydrophobic alpha­helix  membranes spanning region Most have structure similar to nAChR (5 subunits, 4 TM region on each subunit)  Glutamate is the exception unique differences account for ligand binding (Na, K, Ca, Cl  permeability) Heteromeric: 2 or more subunit types Homomeric: 1 subunit type Amino Acid­gated channel: mediate fast synaptic transmission in CNS, involved with many  systems and diseases, pharmacology (describes which transmitters affect them and how drugs  interact with them), kinetics (determine duration of the effect), selectivity (whether they produce  excitation or inhibition and whether Ca+2 enters cell in significant amounts), Conductance  (determines magnitude of effect of open channels)  Glutamate receptors: AMPA (permeable to Na+, K+, not Ca+2, activation = increasing Na+  [depolarization], coexist with NMDA), NMDA (permeable to Ca+2, inward current is voltage,  Ca+2 entry is important to many actions), Kainate (function unknown)  GABA  aAd Gly receptor: GABA does most inhibition in CNS, gly everywhere else, Cl­  channels (Similar to nAChR [alpha binding and beta nonbinding]), modulated by  benzodiazapines (valium) to increase frequency of opening and barbituates (sedatives and anti­ convulsants) to increase channel open time  a. Agonist for Cl­ ion b. Alcohol as well  c. Indicates there are endogenous ligands for benz. and barb. sites, though they aren’t found  (could be neuro steroids)  Ligand gated ion channels: multiple subtypesdistinct pharmacology and electrophysiological  properties, 4 transmembrane regions, ligands binding site @ subunit interface, each subtype with distinctive expression pattern, multiple subunits (pentamer 5 subunits)  G­Protein Coupled receptors and effectors 3 steps 1. Binding of neurotransmitter to receptor protein 2. Activation of G protein  3. Activation of effector systems  7 transmembrane region proteins 2 extracellular loops form binding sites for ligands G protein bind to some of the intracellular loops and are activated upon transmitter binding  100 G protein linked receptor are known G proteins  a. GTP binding proteins  b. 20 kinds  c. 3 subunits (alpha, beta, gamma) GDP bound to G­alpha(inside membrane), activation =  protein split into G­alpha, GTP, and G­beta­gamma (G­alpha converts GTP to GDP  which stops action) d. G­s: stimulatory e. G­i: inhibitory  f. Short cut pathway: binds to ion channel, 30­100 msec time scale, localized, membrane  delimited pathway Second messenger cascades: multiple steps, activation of enzymes Activated G­Proteins can sometimes stimulate multiple pathways Different G­Proteins can have opposite effects Kinases and phosphate involved in many cascades Phosphoralization: protein kinase transfer from ATP floating in cytosol to proteins Dephosphorylation: remove phosphate groups using proteins phosphatases Signal cascades: slow, amplification (long lasting effects), many control points, kinases and  phosphatases involved in many cascades Divergence and convergence in neurotransmitter systems Divergence: ability of 1 transmitter to activate more than 1 kind of subtype of receptor cause  more than 1 type of postsynaptic response Convergence: many transmitter activate different receptors to activate 1 effector system    Structure and Development of the Nervous System (CH. 7 and 23)  Structure of nervous system tell about the function Brain organization: CNS [brain + spinal cord], PNS [nerves]  Central Nervous System [CNS]  1. Brain, spinal cord 2. Cerebrum: rostral­most, largest part of the brain a. Cerebral hemisphere separated by sagittal fissure b. Contralateral: right receives input/controls movement of the left side 3. Cerebellum: behind cerebrum  a. Contains as many neurons as cerebrum  b. Controls movement c. Many connections to cerebrum and spinal cord  d. Right side controls right side [ipsilateral] 4. Relay center, stalk leading to spinal cord and brain a. Regulates body temp, breathing, consciousness b. Most primitive c. Essential to life  5. Spinal cord: encased in vertebral column a. Spinal nerves part of PNS b. Dorsal root: info into spinal cord c. Ventral root      This is part one of the study guide! I’ll post part two of the study guide (the full study guide under my neuro notes! Please check back for the second part! Sorry for any  inconveniences, part two will be up tomorrow. 


Buy Material

Are you sure you want to buy this material for

50 Karma

Buy Material

BOOM! Enjoy Your Free Notes!

We've added these Notes to your profile, click here to view them now.


You're already Subscribed!

Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'

Why people love StudySoup

Steve Martinelli UC Los Angeles

"There's no way I would have passed my Organic Chemistry class this semester without the notes and study guides I got from StudySoup."

Anthony Lee UC Santa Barbara

"I bought an awesome study guide, which helped me get an A in my Math 34B class this quarter!"

Bentley McCaw University of Florida

"I was shooting for a perfect 4.0 GPA this semester. Having StudySoup as a study aid was critical to helping me achieve my goal...and I nailed it!"

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

Become an Elite Notetaker and start selling your notes online!

Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.