drug abuse, addiction

describe the importance of the VTA → nucleus accumbens pathway

facilitates / inhibits transmission at synapses

What is the VTA → Nucleus accumbens pathway called?

mesolimbic (reward/reinforcement pathway)

Other than drugs of abuse, what else activates the mesolimbic pathway? (natural reinforcers)

shopping, food, sex, exercise, gambling, games

what does dopamine release signal to us in the NAcc?

something important (or fantastic) is possibly about to happen

what does cocaine bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

binds to dopamine and NE transporters, blocks them(antagonist), DA and NE in synapse longer

what does THC bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

binds to metabotropic CB1/CB2 receptor, activates it (agonist), inhibitory (decreases ability to release NT), idk last part

what do opioids bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

bind to mu opioid receptors, activates them (agonists), inhibits the cell (pain control, etc.), reinforces DA in VTA → NAcc

what does nicotine bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

binds to nicotinic acetylcholine receptors, activates them (agonist), increases HR & BP & digestion, reinforces DA in VTA → NAcc

what does ecstasy bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

binds to serotonin transporter, blocks and reverses it (antagonist), psychological and perceptual effects

what does amphetamine/methamphetamine bind to and does it activate or block it? what is the resulting effect? how does it increase dopamine transmission in the nucleus accumbens?

binds to DAT, blocks and reverses it (antagonist), vesicles become leaky, DA free in terminal → DA release in synapse

what drugs of abuse are ritalin, adderall, and concerta similar to? in what way?

ritalin and concerta → cocaine (block DAT and NE transporter)

adderall → amphetamine (leaky vesicles and reverse DAT and NE transporters)

what is the effect of opiate action in the pons, midbrain, medulla, and spinal cord?

pons → slow breathing (or decrease stress response)

midbrain → reduce pain perception

medulla → depress breathing & cough reflexes

spinal cord → block pain signal transmission

what drugs are used to treat opiate use disorder and how do they work?

naloxone (narcan) → stops opioid overdose (binds to & blocking opioid receptor)

methadone/buprenorphine → combats opiate addiction (gradual effects, moderate withdrawal)

suboxone

where does nic act in the nervous system?

the brain ?

what are some cognitive effects of nic?

very activating to the cortex & has effects on the PNS

By what neural mechanism is alcohol a stimulant?

increases dopamine in brain

by what neural mechanisms is alcohol a depressant?

inhibits neural activity

what NT systems are responsible for its 1. reinforcing, 2. pleasureful effects?

1. dopamine

2. endogenous opioid

what are some neural and cognitive effects of heavy, chronic use of alc?

changes in white matter, cortical atrophy, damage to hypo & thal & cerebellum, cognitive decline, memory & motor impairments

how do antabuse, naltrexone, and acomprosate work?

antabuse → blocks metabolism of alc (become sick if drink)

naltrexone → blocks opiate receptors so decreases pleasure of drinking alc

acamprosate → glutamate receptor antagonist (protects against withdrawal seizures)

what NT system do LSD, ecstasy, and psilocybin all affect?

serotonin

what hormones does ecstasy stimulate?

oxytocin and vasopressin

what deals mainly with water balance?

vasopressin

what deals mainly with social interactions?

oxytocin

describe the 4 main models of addiction and their weaknesses

moral model → weakness of character & lack of self control (scolding & punishment dont work)

disease model → people need medical treatment rather than punishment (no disease-like physical abnormality has been identified that causes addiction)

physical dependence model → continued use of drugs to avoid unpleasant withdrawal effects (doesn’t explain why addiction develops in the first place or why people still experience cravings after withdrawal)

positive reward model → drugs are reinforcing

what experiences cause cravings / relapse ?

stress, exposure to cues associated w/ drug, drug priming (small exposure)

what experiences can prevent relapse?

environmental enrichment after withdrawal and exposure to non-drug reinforcers

describe the conditioned place preference test and the self-administration test

conditioned → repeatedly receives drug in 1 of 2 places, tendency of subject (drug free) to prefer drug place is assessed

self-administered → subject self-injects drug either into area of brain or general circulation