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Flashcards in Problem 8 Deck (31)
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1

Positive reinforcement

The effect that certain stimuli have on the behavior that preceded them

ex.: smoking makes me feel more alert
--> more smoking

- immediate reinforcing effects can overpower the recognition of longterm aversive effects

2

Operant conditioning

Learning about the consequences of our behavior

--> good consequences = behavior is more likely to be repeated

3

Dopamine

hormone, its release is necessary for a positive reinforcement to take place

--> released into nucleus accumbens

4

Ventral Striatum

Release of dopamine in this region results in the acquisition of a drug taking behavior

- includes the NAC

5

Dorsal Striatum

Release of dopamine in this region results in a behavior that becomes habitual
-- >impulse becomes difficult to resist (automatic)

- includes the Putamen + Basal Ganglia

6

Control of compulsive drug taking behavior

Established by the interactions between the ventral + dorsal striatum

First Time = dopamine is released in ventral striatum

Following times = dopamine is released in dorsal striatum by the stimuli associated with taking the drug

ex.: place, people

7

Dopamine D1 Receptor

causes excitation + facilitates behavior

--> habitual drug use results in an increase in these receptors

8

Dopamine D2 Receptor

cause inhibition + suppresses behavior

--> habitual drug use results in a decrease of them

9

Prefrontal cortex

Judgment, appropriate behavior, risk taking

10

Orexin

- Release in the VTA, NAC, dorsal striatum

- activation when the drug is administered

11

MCH

- located in NAC

- reinforces the effects of drugs

- Inhibited by nicotine (plays a role in hunger)
--> appetite is suppressed by nicotine

12

Negative Reinforcement

Behavior that turns off/reduces an aversive stimulus is more likely to be repeated/reinforced

ex.: Smoking makes the craving for smoking go away
--> more smoking

13

Tolerance

Decreased Sensitivity to a drug which comes from continued use

--> one must take a larger amount of the drug for it to be effective

14

Why do we become tolerant to a drug

- Drugs disturb the normal homeostatic mechanisms in the brain

--> compensatory mechanisms begin to produce effects opposite to those of the drug

15

Withdrawal Symptoms

When person stops taking the drug, compensatory mechanisms make themselves felt even with the absence of the drug

16

Classical Conditioning

Stimuli that have been associated with the drug elicit craving

17

Ventromedial Prefrontal Cortex
(vmPFC)

plays an inhibitory role in reinstatement/relapse

18

Dorsal anterior cingulate cortex

plays an exctitatory role in reinstatement/relapse

--> has excitatory connections with the NAC

19

Locus Coerelus &
Periaqueductal grey matter

plays a role in the production of withdrawal symptoms

20

Cocaine

- dopamine agonist

--> binds w/ receptors + deactivates dopamine transporter proteins = blocks reuptake of dopamine

21

Amphetamine

- dopamine agonist

--> directly stimulates the release of dopamine + blocks the reuptake of dopamine

22

Nicotine

- stimulates ACh receptors + causes dopamine release in the NAC

- reinforcing effect is caused by the activation of the nicotinic receptors in the VTA

23

Physical dependence on Nicotine
(Procedure)

- Nicotinic receptors serve as heteroreceptors on term. but. that release other neurotransmitters; here ACh

1.ACh is released by terminal buttons

2. ACh + Nicotinic Receptors open, entry of calcium

3. Ca+ stimulates the release of ACh + Nicotine

4. Enzyme AChE destroys ACh, but nicotine is not destroyed

5. As levels of nicotine stay steady
--> nicotinic receptors first activate
--> then convert to desensitized state

24

Desensitized State

receptors bind with molecules but don't react to neurotransmitter

--> Smoke doesn't have an effect at some point

25

Insula

larger in smokers, hardens the attempt to quit
--> damage to it makes quitting easier

26

Anxiolytic effect

Doing things one, under normal circumstances, wouldn't do
--> suppressed behavior

27

NMDA Receptor and alcohol

Alcohol acts as an indirect antagonist at NMDA receptors

--> interferes with the transmission of glutamate at NMDA receptors

=> accounts for memory loss

28

GABAa Receptor and alcohol

Alcohol acts as an indirect agonist at the GABAa receptors

--> enhances the action of GABA

=> accounts for anxiolytic effect + sedation

29

THC

produced by marijuhana plant

--> stimulates the release of dopamine

30

CB1 Receptor

site of action of endogenous cannabinoids

--> if blocked; not high

- large numbers are found in the hippocampus which plays a role in memory