Download IB Bio / Neurobiology and Behavior Unit “Drugs of Abuse” Chart

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 possessing 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
Nicotine
(the addictive component in
tobacco, Nicotiana tabacum)
Excitatory or
inhibitory
Benzodiazepines
(Valium™, Xanax™)
Ethanol
Tetrahydrocannabinol
(THC) in Cannabis sativa,
marijuana
(VTA = ventral tegmental area; NA = nucleus accumbens)
effect on
BRAIN?
E
Cocaine
Amphetamines
What is the mechanism of action of the drug on the reward circuit?
Increases dopamine synthesis and release from the VTA neurons onto NA neurons. It does
this because nicotine is an acetylcholine agonist. ACh is released from neurons that excite
VTA neurons.
E
Blocks re-uptake of dopamine by the VTA neurons where they synapse onto NA neurons,
prolonging dopamine stimulation.
E
Increases the release of dopamine from VTA neurons and inhibit re-uptake of dopamine by
VTA neurons. Result: more dopamine in the synapse between VTA and NA neurons.
I
I
The other
chemicals in
tobacco smoke
cause cancer,
etc.
When benzodiazapines interact with the neurons that release GABA, they inhibit them from
release their GABA on VTA neurons. GABA normally inhibits VTA neurons. Inhibiting the
release of inhibitor (“disinhibition”) is like taking your foot off the brakes and allowing your
car to speed ahead. The result is to make VTA neurons fire more & release more dopamine.
Among its many effects on the brain:
 Like benzodiazepines, ethanol inhibits the release of GABA onto VTA neurons, leading
to the 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

I
Other notes of
interest

THC is an agonist of naturally occurring endocannabinoids that bind to CB1 receptors
and are 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 are inhibiting
(with GABA) the VTA neurons. By inhibiting the inhibitors (disinhibition), THC leads to
more dopamine in the NA.
There are fewer
CB1 receptors in
adult brains than
those of teens.
THC dissolves in
myelin.