Behavioral Science (Block 6): Alcohol/substance Abuse 3 & 4

Front 1

how does cocaine affect DA systems in the brain?

Back 1

cocaine binds DA reuptake transporter and keeps dopamine from being reuptaken...this leaves more and more DA at the synapse.this also causes DA post-synaptic receptors to downregulate, causing less DA to be taken up (balance out)

Front 2

how does cocaine affect cerebral perfusion and platelets?

Back 2

cocaine decrease perfusion of blood to the brain (primarily frontal and occipital portions - these 2 areas have worst blood flow, so they lose perfusion first)

cocaine also causes platelets to become extra sticky and plug up small arterioles (can ultimately lead to multi-infarct dementia)

Front 3

which is more of the issue for sx's of cocaine withdrawal: vascular abnormalities or neuronal activity problems?

Back 3

neuronal activity (since withdrawaal from cocaine reduces GABA activity)

Front 4

how do cocaine addicts vs. healthy ppl readct to videos of sad ppl

Back 4

cocaine abusers don't perceive emotions like sadness in others (when compared to healthy ppl) bc their brains aren't activated as much.

however, cocaine abusers get over-aroused when they see others using cocaine (but still not when watching someone feeling sad) because brain actiivty leaves out the frontal cortex (for judgement of the situation). they just want their next touch of cocaine, that's all they care about. they are incapable of processing ability that normal ppl have

Front 5

what is naltrexone's mechanism? how does naltrexone work?

Back 5

it's an opiate antagonist (blocks action of opiates at their receptors).

-reduces cravings
-modifies experience of intoxication
-inhibits priming effect of initial drink (dumbs down the stimulation of craving for more...)

Front 6

what's the relationship b/w alcohol with opiate receptors? what does this have to do with naltrexone?

Back 6

alcohol stimulates opiate receptors by raising beta endorphin levels. cravings start once you stop drinking alochol and levels of beta endorphin drops

when you take naltrexone, it raises beta-endorphin levels (by blocking presynaptic reuptake), blocking alcohol from stimulating opiate receptors - ultimately, relapse is prevented bc alcohol can't raise beta endorphin any further...so you don't get any more stimulation from alcohol (you lose all the "buzz" from drinking)

Front 7

who does naltrexone work for?

Back 7

- ppl who have more severe alcoholism
- ppl with strong family history of alcoholism
- ppl with mu opiate receptor polymorphism

Front 8

how do the beta endorphin levels in sons of alcoholics look? how does naltrexone help?

Back 8

base line levels of beta endorphin have been shown to be much lower in sons of alcoholics (there's more place for effect of a drink of alcohol)

just one drink for ppl with alcoholic families, they get a very big charge of beta endorphin levels in their bodies (it's very rewarding/reinforcing)

**naltrexone attenuates the effects of alcohol on the beta endorphin levels

Front 9

what happens with mice with no mu opioid receptors?

what does this have to do with human alcoholism?

Back 9

they don't self-administer alcohol to themselves...

there's a significant association of A118G polymorphism with alcoholism in humans (more common in northern parts of the world, like Native Americans from Mongolia). LEADS TO 3 FOLD INCREASE IN BETA ENDORPHIN BINDING TO MU RECEPTOR

Front 10

what happens to ppl with this alcoholic polymorphism?

Back 10

1) they have low beta endorphin levels because they have very sensitive receptors
2) when they drink alcohol, they have really high levels of beta endorphin binding to mu opiate receptors

Front 11

what are possible pharmacologic tx's for nicotine dependence?

Back 11

-nicotine patch, gum, lozenge, inhaler, spray
-Bupropion
-nicotine replacement therapy
-varenicline (best so far...)

Front 12

how does varenicline work?

Back 12

partial agonist at the VTA via mu opiate receptor and D2 receptors (at low dosages, it's like nicotine to stimulate VTA; at high dosage, it becomes antagonist and blocks nicotine from having an effect at VTA)

if you start pt at low doses, it feels fine, as you slowly increase dosages, it begins to block.

Front 13

how does selegiline help for tobacco tx?

Back 13

inhibits MAO-A and B...used to treat smoking by substituting this effect of smoking (since one of the chemicals in the cigarettes inhibits MAO and causes anti-depressive effects)

ppl have a better time stopping smoking while being on selegiline bc they don't have the ant-depressive effect taken away so suddenly...

Front 14

T or F. Drugs of abuse are immunogenic.

Back 14

false

Front 15

how do you make a vaccine to nicotine?

Back 15

bind it to cholera toxin and binds nicotine in the blood. so you get immunized to both cholera and nicotine at the same time.

Front 16

why are drugs of abuse drawn to the brain?

Back 16

- they have lots of receptors in the brain
- most of them are lipid soluble and the brain is a good environment

Front 17

what can reduce drug's brain concentration?

Back 17

by increasing antibodies in the blood via a vaccine (ie. nicotine). through the vaccine, you can stop smoking