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

Psych 3313 Week 5 Class Notes

by: Casey Kaiser

Psych 3313 Week 5 Class Notes PSYCH 3313

Marketplace > Ohio State University > PSYCH 3313 > Psych 3313 Week 5 Class Notes
Casey Kaiser
GPA 3.5

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 notes cover week 5 material, the newest material after the first exam.
Behavioral Neuroscience
Dr. Supe
Class Notes
Psychology, Behavioral, neuroscience, brain
25 ?




Popular in Behavioral Neuroscience

Popular in Department

This 8 page Class Notes was uploaded by Casey Kaiser on Sunday September 25, 2016. The Class Notes belongs to PSYCH 3313 at Ohio State University taught by Dr. Supe in Fall 2016. Since its upload, it has received 15 views.


Reviews for Psych 3313 Week 5 Class Notes


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: 09/25/16
Class Notes Week 5 Psych 3313 Psychopharmacology Neurochemicals  Neurotransmitters o Released at directed synapses - it will have a target to act on in the immediate vicinity  Neuromodulators and neurohormones o Neuromodulators can change the way certain things react o Neurohormones typically released into the blood The neurotransmitter classifications are important Acetylcholine (ACh)  Role in the peripheral nervous system o Autonomic - both pre-ganglionic, parasympathetic post-ganglionic o Somatic - neuromuscular junction, main neurotransmitter at a neuronal junction  Central Nervous System o Projections from basal forebrain to hippocampus and amygdala, septal area, brainstem  Behaviors o Autonomic functions, movement, learning and memory  Clinical conditions o Alzheimer's disease, myasthenia gravis, schizophrenia? How do we make and break down Ach  Made with the combo of choline +acetate via enzyme choline acetyltransferase - typically called ChAT There are two main subtypes of receptors for Ach  Nicotinic (ionotropic)  Muscarinic (metabotropic) Degradation  Reuptake or broken down by enzyme (AChE) Major releasing centers -  Basal forebrain, smaller area but can project to the entire forebrain o Damage here in Alzheimer's Disease o Means that there is less acetylcholine being released, severe memory loss is a symptom of this disease  Cholinergic nuclei to the pons and brainstem Nicotinic Ach Receptor  Binds nicotine  Blocked by curare o A plant based poison, our muscles cannot respond to messages and will not contract  Ionotropic receptor o Quick, short time being active  Located at neuro muscular junction, autonomic nervous system, and central nervous system  Excitatory, this junction will open with the presence of acetylcholine and sodium will come in, causing muscles to contract  Post-synaptic Muscarinic ACh Receptor  Binds muscarine  Blocked by atropine o Other variations of chemicals can be used o Atropine is used in eye exams  Metabotropic receptor - GPCR  Response is slower and prolonged, amplified  Found on Myocardial and smooth muscles, in the heart, digestive system and central nervous system  Mediates inhibition and excitation in target cells - it depends on the subtype that is involved  Both pre and post synaptic, more common on post synaptic Small Molecule NTs: Monoamine Neurotransmitters Catecholamine's - dopamine, norepinephrine, epinephrine  Synthesized from tyrosine Indolemines - Serotonin, melatonin  Synthesized from tryptophan Histamine Catecholamine's Synthesis  Start with tyrosine - found abundantly in the diet (enzymatic step involving Tyrosine Hydroxylase)  Enzymatic step turns it into I-dopa  Step into dopamine  Step into norepinephrine  Stop into epinephrine Rate limiting step - Tyrosine Hydroxylase, this step determines how much of the rest we can make L-dopa as potential treatment for Parkinson's Disease - increasing overall amount of dopamine available Dopamine (DA)  Role in the peripheral nervous system o Neuromodulator for other NTs  Role in central nervous system o Substantia Nigra releases dopamine to the basal ganglia o Ventral tegmental area projects to the hippocampus, amygdala, nucleus accumbens, and frontal lobe  Behaviors o Movement control, reinforcement, planning  Clinical conditions o Parkinson's disease, schizophrenia, drug abuse Synthesis - made with tyrosine hydroxylase Receptors  D1, D5 - stimulatory, metabotropic G-protein coupled receptors  D2, D3, D4 - inhibitory G-protein coupled receptors Degradation  Enzymes Monoamine Oxidase (MAO), catechol-O-methyl transferase (COMT), and aldehyde dehydrogenase, act in sequence to break down dopamine Projection Areas in the Brain  Ventral tegmental area - reward system  Substantia Nigra - motor system Norepinephrine (NE) / Noradrenaline  Role in peripheral nervous system o Autonomic - sympathetic post-ganglionic synapses  Signal to increase heart rate, breathing, any fight or flight changes  Role in central nervous system o Widespread projection from Pons (Locus Coeruleus), medulla, hypothalamus  Behaviors o Arousal and vigilance (high attention), mood  Clinical conditions o Depression, mania, PTSD  Synthesis o Made from dopamine  Receptors o Alpha and beta  Alpha -  Beta - blockers, can block certain symptoms of anxiety, quickened heart-rate, shaking, etc..  Degradation o Enzymes monoamine oxidase, catechol-O-methyl transferase, and aldehyde dehydrogenase, acting in sequence to break it down o Pretty much the same as dopamine Projections  Locus Coeruleus - to pretty much the entire brain o Probably release more in times of stress Epinephrine/adrenaline  Relatively minor role in brain, strong neurohumoral effect  Adrenergic neurons  Regulation of blood pressure, eating Serotonin (5HT)  Role in the PNS o Enteric - digestive motility  Role in CNS o Widespread projection from Pons (raphne Nucleus) to brain and spinal cord  Behaviors o Sleep-wake cycles, appetite, mood, aggression, social rank  Clinical conditions o Depression, OCD, alcoholism, pretty much any mood or anxiety disorder "Serotonin is involved in everything but responsible for nothing"  Synthesis o Made from tryptophan  Receptors o At least 15 types and sub-types o Most are metabotropic, can be excitatory or inhibitory  Degradation o Reuptake - SSRIs block reuptake o Monamine Oxidase  Projections o Raphe Nuclei Histamine  Synthesized from histidine  Projections from basal posterior hypothalamus, Mast cells  Associated with wakefulness - like how Benadryl makes someone sleepy Amino Acids Neurotransmitters  GABA o Main inhibitory nt in the brain o Mood - especially anxiety o Involved in seizures  Glutamate o Main excitatory nt in the brain o Long-term memory o May be associated with neurotrauma like spinal cord damage Glutamate Synthesis and Removal  Made from the Kreb's Cycle  Isolation of the synapse with astrocytes o Astrocytes are critical in removing glutamate Glutamate Receptors  Ionotropic o AMPA - most common, excitatory opens sodium channel o Kainate - opens sodium channel o NMDA -open sodium and calcium channel  Metabotropic NMDA Glutamate receptor  Glutamate is not enough to open the NMDA channel  The channel is both ligand gated and voltage gated  Potentially excitotoxic o Opens too much, lets too much in and can lead to cell death GABA synthesis and removal  Generally inhibitory  It is synthesized and derived from glutamate  Glutamic Acid Decarboxylase (GAD) is the enzyme that synthesizes GABA  Terminated by high-affinity uptake systems in Neurons and Glia  Likely involved in epilepsy and anxiety disorders o Medicated for dogs to prevent seizures for them (typically larger dogs) GABA Receptors  Synthesized from glutamate  GABAa - ionotropic o Open and allow chloride to come in o It has many different molecular recognition sites, many different binding sites  GABAb - metabotropic o Gates the potassium channel Glycine  Role in the Central Nervous System o No major direct role In the brain, more in the spinal cord o Major inhibitory NT in the spinal cord o Excitatory co-activator at NMDA glutamate  Behaviors o Sleep wake cycles  Toxins o Strychnine - umbrella murder ATP and Adenosine  Act in the CNS and connections between autonomic neurons and the vas deferens, bladder, heart, and gut  ATP is associated with pain perception and sleep-waking cycles  Adenosine inhibits the release of many neurotransmitters - how caffeine works, blocks these receptors Peptides  Endorphins o Reduce pain and enhance reinforcement, feelings of well-being o Associated with the "runners high" o The morphine within  Substance P o Transmitter in spinal cord neurons sensitive to pain  Insulin and cholecystokinin o Digestive functions o Different amounts of these will influence food response  Oxytocin and vasopressin o Neuromodulators and neurohormones o Associated with childbirth and love o Have a lot to do with relationships and social interactions Gaseous Neurotransmitters  Diffuse through membranes and interact with intracellular receptors  They work backwards - the signal goes from post-synaptic to pre-synaptic, retroactive  Nitric Oxide o Found in CNS and PNS, smooth muscle o Relaxes smooth muscle cells and blood vessels o Can cause erection  Carbon monoxide o Deadly o Can make you go crazy or kill you What is a drug? Any substance that alters the body or its functions  We have a communal understanding that a drug is used as medicine, recreation, enhancement, or abuse but it can be anything They can be divided into -  Agonist - "acts like" o Either going to mimic or enhance effects of NT o Activate receptor o Block reuptake or degradation - more of NT is available, larger effect  Antagonist - "bad guy" o Blocks or decreases the effect of the NT o Competitive or non-competitiv o Blocks receptors without activating o Decreases the availability of Nt by reducing the effect Effects of agonists  Affinity - how strongly the agonists binds to the receptor o NOT MAGNETISM but you can kind of think of it this way  Potency - amount of the drug needed to make a response o More potent drug has more power  Efficacy - how much of this agonist is going to produce its effect o Partial agonist will be similar to a NT but has some slightly different properties, so maybe the channel Is not open as long Dose Responsive Curves  Logarithmic Curves  The ED50 is the effective dose for 50% of the population o When looking at medication something that only works for 50% of the people is also not working for 50%  When the option to take the medication comes with a lower or higher dose, typically people want to take the lower dose  A lot of drugs will not effect one receptor, typically they will bind to other receptors as well, and that is how side effects come into play Therapeutic Index  Effective dose over the toxic dose o The difference between where the effective dose and the toxic dose for 50% of the population is called the margin of safety  The public typically wants a larger margin of safety  We start low with a dosage, see what the response is and slowly raise it until we find the effects we want. If there are no responses they must be in the 50% who do not respond to a certain drug Sites of Drug Action  Every step in the life of a NT is a step that a drug can be involved  Anything presynapse is typically indirect Post-synaptic receptor effects  You can change the affinity or potency  You can change different qualities of the receptor not just block Drug interactions at Cholinergic Synapse ****  Test self with the steps; synthesis, storage, release, breakdown, and action Drug interactions at the Dopamine Synapse Drug interactions at the Serotonergic Synapse Basic Principles of Drug Effects  Administration of drugs o Method of administration leads to different effects of the nervous system o Don’t forget the blood-brain barrier  Most drugs are used because they are good at surpassing the BBB  Individual differences o Body type, weight, sex, and genetics o People will react to drugs differently  Placebo effects o User expectations influence drug effects  This can result in real biochemical and physiological effects in the brain\  If people think they are ingesting something and truly believe it, it can have the same effects on them as if they had actually consumed the substance  Tolerance o Decreased response to a drug with repeated use o 3 types  Metabolic - breakdown processes can change  Liver enzymes  Functional - receptors for NT can down regulate or up regulate changing the drug response  Learned - Wenger  Body may be more practiced later after more use even though it is impaired in the same way  Withdrawal o Occurs when the substance use is discontinued, opposite effect can be caused by discontinued drug o Your body develops a response to a drug so when it is not there it wants that drug more  Addiction o Characterized by compulsive need to re-administer a drug despite the harm o There are so many aspects to addiction from many different fields


Buy Material

Are you sure you want to buy this material for

25 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."

Allison Fischer University of Alabama

"I signed up to be an Elite Notetaker with 2 of my sorority sisters this semester. We just posted our notes weekly and were each making over $600 per month. I LOVE StudySoup!"

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!"


"Their 'Elite Notetakers' are making over $1,200/month in sales by creating high quality content that helps their classmates in a time of need."

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.