Psychobiology - Ex2 - Ch3/4

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events involved in synaptic transmission

Back 1

1. AP arrives @ pre-syn axon terminal 2. Depolarization; voltage-gated Ca channels in terminal membrane open, Ca ions enter 3. Ca ions cause synaptic vesicles with NT to fuse with pre-syn membrane and rupture, releasing NT into synaptic cleft 4. NT molecules bind to receptor molecules in post-syn membrane > ion channels open > E/IPSP 5. E/IPSP in post-syn cell spread toward axon hillock (> AP) 6. Synaptic transmission rapidly stopped 7. NT may activate pre-syn receptors, decreasing NT release

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ligand

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substance that binds to a receptor

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ACh

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acetylcholine - first NT to be discovered; found in ANS, motor systems, brain

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number of sub-types of receptors on which ACh acts

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four

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cholinergic

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refers to cells using ACh as their NT

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(NT) receptor

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protein that captures and reacts to molecules of NT or hormone

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post-syn receptor determines action of NT

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ACh can be excitatory or inhibitory at different synapses

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agonist

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molecule which binds to a receptor, initiates response

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example of agonist

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nicotine (mimics ACh)

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antagonist

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molecule which binds to a receptor, interferes with normal response

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examples of antagonists

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curare, bungarotoxin (block ACh receptors)

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agonist drug effects

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increase synthesis of NT, increase NT by destroying degrading enzymes, drug binds to auto-receptors and blocks inhibitory effect on NT release (increases net release), drug binds to post-syn receptors and activates/increases effect, block deactivation of NT by blocking re-uptake

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antagonist drug effects

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block synthesis of NT, cause NT to leak from vesicles and be destroyed by enzymes, block release of NT from terminal buttons, activate inhibitory effect on NT release (decreases net release), act as receptor blocker: bind to post-syn receptor and block effect of NT

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processes that bring transmitter effects to a halt

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degradation, reuptake

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degradation

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breakdown of NT into inactive metabolites (e.g., AChE)

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reuptake

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process by which released synaptic NT are re-absorbed by pre-syn neuron via transporters (pre-syn receptors)

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endogenous vs. exogenous

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internal, external (to body)

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exocytosis

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cellular process resulting in release of substance into extracellular space (i.e. NT into synaptic cleft)

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types of NT receptors

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ionotropic, metabotropic

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ionotropic receptor

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fast; quickly changes shape or open+close ion channel when NT binds

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metabotropic receptor

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slow; alters chemical Rx in cell, uses 2nd messengers to open ion channel; may also start chemical Rx to change gene expression

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NT criteria

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substance synthesized in pre-syn neurons, stored in axon terminals, released when AP reaches axon terminals, recognized by receptors of post-syn membrane, causes change in post-syn cell, blocking release interferes with effects on post-syn cell

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types of NTs

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amine, amino acid, peptide, gas

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amine NTs

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acetylcholine, dopamine, norepinephrine, serotonin

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acetylcholine (ACh)

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found in ANS, motor systems, basal forebrain; loss of neurons associated with Alzheimer's

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dopamine (DA)

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mesostriatal- substantia nigra, associated with motor control (loss of neurons > Parkinson's); mesolimbocortical - ventral tegmental area, associated with learning shaped by positive reinforcement

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norepinephrine (NE)

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found in locus coerueleus, lateral tegmental area; control of behaviors (e.g. alertness, mood, sexual behavior);

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serotonin (5-HT)

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found in midline of midbrain and brainstem, raphe nuclei; associated with mood, anxiety, sleep

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amino acid NTs

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glycine, glutamate, GABA

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glutamate

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excitatory NT, works through NMDA receptors

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GABA (gamma-aminobutyric acid)

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inhibitory NT; GABA-A: ionotropic, mimicked by benzodiazepines (e.g. Valium, Ativan, used to reduce anxiety)

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peptide NTs

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found in gut, spinal cord, brain; opioids mimic opiate drugs, reduce perception of pain (e.g. morphine); oxytocin, vasopressin

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gas NTs

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produced outside axon terminals, diffuses upon production, activates 2nd messengers, no receptors involved, can act as retrograde NT; nitric oxide, carbon monoxide

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(binding) affinity

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degree of chemical attraction between ligand and receptor

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efficacy/intrinsic activity

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ability of bound ligand to activate receptor

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DRC

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dose-response curve: graph of relationship between drug doses and effects

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tolerance

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condition in which repeated exposure to drug causes decreasing responsiveness to constant dose

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metabolic tolerance

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organ systems become more effective at eliminating drug

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functional tolerance

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target tissue shows altered sensitivity by changing # of receptors (i.e. down-/up-regulation)

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down- vs. up-regulation

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decrease vs. increase in receptor availability to agonist vs. antagonist

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cross-tolerance

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tolerance for once drug generalize to others in its class

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effects of drugs on pre-syn processes

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TRANSMITTER PRODUCTION (inhibition of NT synthesis, block of axonal transport, interference with NT storage), TRANSMITTER RELEASE (prevention of synaptic transmission (APs), alteration of synaptic NT release, modulation of pre-syn NT release (blocked autoreceptors)), TRANSMITTER CLEARANCE (inactivation of NT reuptake, degradation)

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effect of drugs on post-syn processes

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blockade/activation of receptors, alteration of # of post-syn receptors, modulation of second messengers

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functional classes of psychoactive drugs

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relieve severe symptoms (antischizophrenics, antidepressants, anxiolytics, opiates), alter consciousness (tobacco, alcohol, marijuana, hallucinogens)

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antischizophrenics

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reduce synaptic activity; neuroleptics/antipsychotics (antagonists of DA receptors), atypical neuroleptics (block serotonin receptors)

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antidepressants

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increase synaptic transmissions; monoamine oxidase (prevent breakdown (thus prolonging activity) of MA NTs (DA, 5-HT, NE), tricyclic (block reuptake of 5-HT, NE), selective serotonin reuptake inhibitors (act specifically at serotonergic synapses)

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anxiolytics

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decreases excitability of neurons; depressants (reduce nervous system activity), barbiturates (reduce anxiety, promote sleep, avoid seizures), benzodiazepines (agonists on GABA-A receptors)

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opiates

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analgesic (painkiller); e.g. morphine, heroin, codeine, which bind to opiate receptors, especially in periaqueductal gray; endogenous opioids: enkephalins, endorphins, dynorphins

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tobacco

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contains nicotine, which acts as a stimulant, increasing heart rate, blood pressure, digestive action; agonist on nicotinic ACh receptors in ventral tegmental area (positive reinforcement)

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alcohol

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biphasic effect: stimulant, depressant; agonist on GABA receptors; affects frontal lobe, reduces rate of neurogenesis; dementia, fetal alcohol syndrome, Wernicke-Korsakoff syndrome, cardiovascular problems, liver damage, ...

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marijuana

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contains delta-9-tetrahydrocannabinol, effects vary; receptors found in substantia nigra, hippocampus, basal ganglia, cerebellum, frontal cortex; endocannabinoid (analog produced in brain): anadamide

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stimulants

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excitatory: increase excitatory APs, decrease inhibitory processes; caffeine (blocks pre-syn adenosine receptors (which decrease NT release, resulting in net NT increase), cocaine (blocks blocks reuptake of MA NT), synthetics e.g. amphetamine (increases MA NT release, decreases breakdown of NT once released)

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hallucinogens

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alter sensory perception; LSD (activates visual cortex 5-HT receptors), MDMA (changes levels of DA)

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hallucinogens: dissociatives

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produce feelings of depersonalization, detachment from reality; antagonists on NMDA-type glutamate receptors; e.g. PCP, Special K

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substance-related disorders

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dependence (desire to self-administer), substance abuse (pattern of use not fully meeting previous criteria)

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models of drug abuse

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moral (blames abuser for lack of moral character, self-control), disease (abuse requires medical treatment), physical dependence (abuse uses drug to avoid withdrawal, dysphoria), positive reward (drug use is controlled by positive reinforcement)

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drug abuse treatment

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detoxification (ease withdrawal symptoms), agonist/analogs (partially activate same pathways to wean); antagonists (block effect of drug), metabolism-altering, reward-blocking, anticraving, immunization (antibodies remove drugs from circulation before reaching brain)