PSYC304 Exam 3

Direct Agonist

binds directly to same bonding site as endogenous neurotransmitter, activates it

Indirect Agonist

binds to different site, activates receptor

Direct Antagonist

actively binds to receptor, does not activate it

Indirect Antagonist

binds to alternative site, changes receptor, does not activate it

Peripheral Administration

intromuscular, oral, intranasal, intravenous

Intracerebral

injected directly into the brain

Intrathecal

get to CSF through subarachnoid space around spinal cord or brain

Intracerebroventricular

through ventricles (ex. chemo)

Potency

amount of drug necessary to produce a biological response of a certain magnitude

Affinity

how well ligand binds to receptor

Effective Dose (ED50)

dose required to produce 50% of effect → potency

higher potency = low on the dose-response curve

Lethal Dose (LD50)

dose that leads to the death of 50% of subjects

Therapeutic Index

margin of safety, goal of research to optimize this

Tolerance

decrease in potency as the drug is administered more frequently

Naloxone (Narcan)

opiate antagonist, high affinity for opiate receptor, knocks opioids out of the way and take their place

Sensitization

increase in the effectiveness of a drug that is administer repeatedly

Presynaptic Acetylcholine Drugs

dietary choline, black widow venom, boton

Postsynaptic Acetylcholine Drugs -

nicotine, curare, muscarine, atropine

Acetylcholinesterase

enzyme that breaks down acetylcholine

Nicotinic Acetylcholine Receptors

ionoptropic, bind nicotine, mediate transmission → neuromuscular junction

spinal cord to smooth muscles

Muscarinic Acetylcholine Receptors

metabotropic (G-protein) ← most prevalent, autonomic nervous system

slow the heart

Atropine

blocks muscarinic receptors, reduce siliva production

Curare

blocks ACh receptors → paralysis

Black widow venom

promotes ACh release, hyperactivity → reduced regulation, uncontrollable muscle movement

Adenosine

product of enzymatic degradation of ATP

made by neurons + glial cells

accumulates during wakefulness and reduces during sleep

neuromodulator: neuronal inhibition, sleep

Adenosine receptors

metabotropic

caffeine(stimulant): direct antagonist for adenosine receptors

Glutamate AMPA Receptor

mediates fast EPSP in brain/spinal cord

multi-sub unit, oligomer

permeable to Na+, not Ca2+

Glutamate NMDA Receptor

6 different binding sites

channel passes both Na+ and Ca2+

plasticity/excitoxicity

glycine, Mg2+, PCP, ketamine

Glycine

excitatory co-agonist → needs glutamate + glycine

Mg2+ Block

site sucks in an Mg2+, no Na+ or Ca2+ can get in

Phencyclidine (PCP)

indirect antagonist, shuts down excitatory transmission, leads to psychosis

Ketamine

indirect antagonist, antidepressant

GABAa Receptors

ionotropic receptors

when GABA binds → leads to influx of Cl- = hyperpolarization

Vitamin B

deficiency = diminished GABA synthesis

can lead to seizures + death in infants

GABA Agonists

Benzodiazepines, Barbituates

Benzodiazepines

anti-anxiety + mmuscle relaxants

increase frequency of channel being open

Barbituates

anesthesia + control of epilepsy

prolong duration of open channel

Picrotoxin

pro-convulsant

decreases time channel is open

Types of Monoamine Transmitters

dopamine and serotonin

modulatory effects w/ G-protein receptors

Meso/nigrastraital Dopamine Pathway

SN → Striatum

voluntary movement

degeneration = parkinson’s → L-dopa helps treat it

Mesolimbic Dopamine Pathway

VTA → Limbic System

motivation, reward

drug abuse + schizophrenia

Mesocortical Dopamine Pathway

VTA → PFC

emotion, exec functions

could be dysfunctional in schizophrenia

Tyrosine Hydroxylase

converts tyrosine into L-dopa

D1 Receptors

D1 and D5

stimulatory, increase cAMP, increase PIP2 hydrolysis

D2 Receptors

D2, D3, D4

inhibitory, decrease cAMP, increase K+, decrease voltage-gated Ca2+

classical antipsychotic drugs = antagonists

Dopamine-related Addiction

cocaine, amphetamine, methylphenidate = inhibit dopamine reuptake by blocking dopamine transporter

repeated exposure can have long-lasting effects on pathways

Raphe Nuclei

serotonigergic cell body location

Tryptophan

precursor of serotonin

synthesized into serotonin in axon terminal

LSD

(serotonin) 5-HT2 partial agonist

Monoamine Hypothesis

deficiency of norepinephrine + serotonin causes depression

Iproniazid

developed to treat tuberculosis (MAOi)

depression = decrease monamine transmitters

Reserpine

treats hypertension

interferes with storage of serotonin

Tricyclic Anti-depressants

block 5-HT reuptake

Monoamine Oxidase (MAO)

enzymes that break down monoamine neurotransmitters + dietary amines

oxidation

Monamine Oxidase Inhibitors (MAOis)

prevents the break down of monoamine neurotransmitters (serotonin, norepinephrine, dopamine)

Endorphin

combination of endogenous and morphine

built in stress relievers and painkillers

respiratory depression

Dynorphin

regulate stress, mood, pain, addiction

sedation, dysphoria, aversion

Enkephalin

short chain of 5 amino acids

neurotransmitter and neuromodulator to regulate pain perception

convulsions and hyperlocomotion

Mu opioid receptor (MOR)

endorphin receptor

Fentanyl

synthetic opioid

direct agonist

Morphine

direct agonist for mu opioid receptor