Problem 8 Flashcards
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
Operant conditioning
Learning about the consequences of our behavior
–> good consequences = behavior is more likely to be repeated
Dopamine
hormone, its release is necessary for a positive reinforcement to take place
--> released into nucleus accumbens
Ventral Striatum
Release of dopamine in this region results in the acquisition of a drug taking behavior
- includes the NAC
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
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
Dopamine D1 Receptor
causes excitation + facilitates behavior
--> habitual drug use results in an increase in these receptors
Dopamine D2 Receptor
cause inhibition + suppresses behavior
--> habitual drug use results in a decrease of them
Prefrontal cortex
Judgment, appropriate behavior, risk taking
Orexin
- Release in the VTA, NAC, dorsal striatum
- activation when the drug is administered
MCH
- located in NAC
- reinforces the effects of drugs
- Inhibited by nicotine (plays a role in hunger)
- -> appetite is suppressed by nicotine
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
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
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
Withdrawal Symptoms
When person stops taking the drug, compensatory mechanisms make themselves felt even with the absence of the drug
Classical Conditioning
Stimuli that have been associated with the drug elicit craving
Ventromedial Prefrontal Cortex
vmPFC
plays an inhibitory role in reinstatement/relapse
Dorsal anterior cingulate cortex
plays an exctitatory role in reinstatement/relapse
--> has excitatory connections with the NAC
Locus Coerelus &
Periaqueductal grey matter
plays a role in the production of withdrawal symptoms
Cocaine
- dopamine agonist
- -> binds w/ receptors + deactivates dopamine transporter proteins = blocks reuptake of dopamine
Amphetamine
- dopamine agonist
- -> directly stimulates the release of dopamine + blocks the reuptake of dopamine
Nicotine
- stimulates ACh receptors + causes dopamine release in the NAC
- reinforcing effect is caused by the activation of the nicotinic receptors in the VTA
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
- As levels of nicotine stay steady
- -> nicotinic receptors first activate
- -> then convert to desensitized state
Desensitized State
receptors bind with molecules but don’t react to neurotransmitter
--> Smoke doesn't have an effect at some point
Insula
larger in smokers, hardens the attempt to quit
–> damage to it makes quitting easier
Anxiolytic effect
Doing things one, under normal circumstances, wouldn’t do
–> suppressed behavior
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
GABAa Receptor and alcohol
Alcohol acts as an indirect agonist at the GABAa receptors
--> enhances the action of GABA
=> accounts for anxiolytic effect + sedation
THC
produced by marijuhana plant
--> stimulates the release of dopamine
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
Cannabidiol
CBD
- antagonist
- not reinforcing –> not high=> opposite to THC
