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Welcome to 2-minute neuroscience, where I explain neuroscience topics in 2 minutes or
In this installment I will discuss nicotine.
Nicotine is the main psychoactive component of tobacco.
It primarily exerts its effects by activating, or acting as an agonist, at certain receptors
for the neurotransmitter acetylcholine.
These receptors, known as nicotinic acetylcholine receptors, are found throughout the central
and peripheral nervous systems.
When nicotine binds to nicotinic acetylcholine receptors, it typically causes depolarization
of the neuron they are found on and the resultant release of a variety of neurotransmitters.
Nicotine’s action at acetylcholine receptors is thought to be the starting point for the
drug’s behavioral effects, but exactly how it produces these effects is not completely
Nicotine’s rewarding and addictive qualities are thought to be linked to its ability to
cause increased dopamine levels in areas like the nucleus accumbens.
Nicotine also increases acetylcholine release, which might contribute to the enhanced attention
and cognitive function associated with its use.
And its ability to increase norepinephrine activity might contribute to the heightened
arousal caused by the drug.
In all of these effects, however, it’s likely multiple neurotransmitter systems are involved.
Nicotine also acts on nicotinic acetylcholine receptors in the peripheral nervous system,
where it can lead to increased sympathetic nervous system activity like an elevated heart
rate and blood pressure.
It also causes the increased release of catecholamines like epinephrine from the adrenal glands,
which can further enhance this sympathetic activity.
Although nicotine first activates nicotinic acetylcholine receptors, it subsequently causes
the receptors to become desensitized, or less responsive, increasing tolerance to repeated
uses of the drug.
As more receptors become desensitized, the brain tends to upregulate, or add more, acetylcholine
These increased receptor numbers might play a role in the withdrawal and craving that
occurs when nicotine administration is ended.