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1) Present the mild to moderate dose behavioral and subjective effects of cocaine
and compare with the high dose behavioral and subjective effects.
2) Present the evidence that the mesolimbic dopamine pathway plays a major role in
the rewarding aspects of cocaine.
a. Table 11.2
b. Regions of NA
c. Knockout mice?
i. Model implies more than mesolimbic pathway involved
but………..
d. Human brain imaging
i. PET scan
ii. Drug occupancy of DAT
iii. Occupancy rate
iv. Baseline DA activity
e. Evidence for the involvement of DA receptor subtypes
3) Discuss tolerance and sensitization effects of psychostimulant use
a. Chronic vs acute exposure?
b. Acute tolerance with long-term sensitization
i. Animal data
ii. As a model of human drug use
c. Phases of sensitization (include hypothesized synaptic events)
i. Induction
ii. Expression
4) Describe the mechanism of action of the Amphetamines (triple whammy)
5) Discuss MDMA (ecstasy)
a. Brief history
b. Psychological effects
c. Physiological effects
d. Mechanism of action
e. Neurotoxicity?
i. Animal
ii. Human
6) Describe how the endocannabinoids work
a. Receptor
i. Metabotropic or ionotropic
ii. Inhibitory or excitatory – explain why
iii. Where located
b. Endocannabinoids
i. Where produced?
ii. Why produced?
iii. Storage?
c. Depolarization induced suppression of inhibition
i. Explain this using a hippocampal pyramidal neuron and GABA
interneuron as an example
d. Depolarization induced suppression of excitation
i. Just define and indicate the NT used by the interneuron
e. Evidence for the role of endocannabinoids in DSI
7) Describe the 4 phases of acute subjective effects of marijuana (Iversen, 2000).
Describe the acute physiological effects of marijuana. Describe the evidence that
CB1 receptors are at least partially involved in the subjective and physiological
effects of marijuana.
8) Discuss the various potential therapeutic effects of marijuana that have been
posited. Include evidence for each.
a. Antiemetic
b. Appetite stimulant
c. Pain relief
d. Others?
e. Why has the development of cannibinoid medications been slow?
9) Discuss the various deficits that acute cannabinoid exposure is associated with.
Include the following topics
a. Human deficits
i. Verbal
ii. Spatial
iii. Time estimation
iv. Explicit memory
v. Psychomotor performance
b. Behavioral "cognitive" tolerance
c. Animal studies
i. Tasks
ii. Reversal learning
1. perseveration
a. potential brain region
10) Discuss the evidence related to the reinforcement value, addiction potential, and
potential long term effects of cannabis use.
a. Reinforcing for humans?
b. Reinforcing for animals?
c. Involvement of the mesolimbic system?
d. Cannibinoid and DA system
e. Does cannabis use produce tolerance?
i. Humans
ii. Animals
f. Does cannabis use produce dependence?
g. Effects of chronic cannabis use
i. Amotivational syndrome?
ii. Physiological?
1. lungs
2. immune
3. reproduction
11) Discuss the background and history of the different hallucinogens. Mescaline,
Psilocybin, DMT, 5-MeO-DMT, and LSD. Present the subjective and
physiological response to hallucinogens.
12) Describe the evidence for the involvement of 5-HT receptors in the effects of
hallucinogens
a. Which receptors does LSD bind with
b. How was it originally determined that 5-HT2A and 5-HT2C played a role?
c. Discuss Vollenweider's psilocybin and antagonist study
d. Discuss drug discrimination with antagonist work
13) Discuss the theories for how hallucinogens cause hallucinations
14) Discuss PCP and Ketamine
a. What are the subjective effects?
b. What's the evidence regarding reinforcement?
c. How does PCP and ketamine work synaptically?
d. Discuss PCP and ketamine as a model for schizophrenia
Shorter Answer
Why wasn't cocaine smoked very often prior to the 1980s; what changed that?
How do the different routes of administration affect plasma levels of cocaine?
Cocaethylene
How does cocaine work at the synapse (make sure to include NTs and relative affinities)?
Cocaine psychosis
Self administration of cocaine (generalization to other drugs)?
Explain the significance of generalization or lack of generalization
Sympathomimetic
Cocaine effects on fetal development?
Pharmacotherapy for cocaine?
Therapeutic uses of amphetamines
Evidence for calming effects of amphetamines?
Evidence for neurotoxic effects of amphetamines
Animal studies
Human studies
Forms of Cannabis
Routes of administration of cannabis
Brain areas with a high distribution of cannabinoid receptors
THC
SR 141716
Rimonabant
Anandamide
Endocannabinoids
How are endocannibinoids deactivated from the synapse?
Fatty acid amide hydrolase (FAAH)
Indolamine hallucinogens
Phenethylamine hallucinogens
Discuss tolerance to hallucinogens
Are hallucinogens addictive? Do they cause overdose?
Explain