Download “Drugs of Abuse” Chart, Neil 9e KEY

IB Bio / Neurobiology and Behavior Unit
“Drugs of Abuse” Chart, Neil 9e KEY
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All of these drugs co-opt the brain’s reward pathway, the circuitry normally activated by environmental stimuli having survival value: food, water, mates.
An agonist is a chemical that binds to a receptor and activates the receptor to produce its normal biological response; an antagonist also binds to the receptor,
but it inhibits it, blocking the normal response.
Drug
Excitatory or
inhibitory
(the addictive component in
tobacco, Nicotiana tabacum)
E
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
E
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Increase the release of dopamine from VTA neurons & inhibit re-uptake of dopamine too.
Result: more dopamine stimulation.
I
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
Neurons releasing GABA normally inhibit VTA neurons.
Benzodiazapines stop these neurons from releasing their GABA onto VTA neurons.
Inhibiting the release of inhibitor (“disinhibition”) is like taking your foot off the brake,
allowing your car to speed.
Result: VTA neurons fire more and release more dopamine.
Amphetamines
(Valium™, Xanax™)

Tetrahydrocannabinol
(THC) in Cannabis sativa,
A.K.A. marijuana
The other
chemicals in
tobacco smoke
cause cancer,
etc.
Blocks re-uptake of dopamine by the VTA neurons which synapse onto NA neurons,
prolonging dopamine stimulation.
E
Ethanol
Increases dopamine synthesis and release from VTA neurons onto NA neurons because
nicotine is an acetylcholine agonist.
ACh is the NT released from neurons that excite VTA neurons.

Cocaine
Benzodiazepines
Other notes of
interest
(VTA = ventral tegmental area; NA = nucleus accumbens)
effect on
BRAIN?
Nicotine
What is the mechanism of action of the drug on the reward circuit?
I
I
Among its many effects on the brain:
 Like benzodiazepines, ethanol inhibits the release of GABA onto VTA neurons, leading to
VTA neurons firing more rapidly and releasing more dopamine in the reward system.
 High doses of ethanol depress brain regions for coordination, balance and pain
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
THC is an agonist of naturally occurring endocannabinoids that bind to "CB1 receptors"
involved in appetite, pain sensation, mood, and memory.
THC increases extracellular dopamine concentrations in the NA. How this occurs is
unclear. It might be that THC binds to CB1 receptors on neurons that were inhibiting
(with GABA) the VTA neurons. Through disinhibition, THC increases dopamine in NA.
There are fewer
CB1 receptors in
adult brains
than those of
teens.
THC dissolves
in myelin.