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Nicotine, the primary psychoactive components of tobacco smoke, produce diverse neurophysiological and behavioral effects through several brain regions and neurochemical pathways. It acts as an agonist to activate and desensitize nicotinic acetylcholine receptors. Nicotinic signaling leads to activation of reward centers in the CNS, including the mesoaccumbens dopamine system, which ultimately leads to behavioral reinforcement and addiction. Indeed, the actions of nicotine on many systems, including brainstem cholinergic, GABAergic, glutaminergic, noradrenergic, and serotonergic systems, may help to mediate nicotine effects related to addiction. And many years of smoking induces neuroadaptations in acetylcholine and dopamine systems. Moreover, the long-term synaptic changes results in learned behaviors and memory which are associated with smoking. We reviewed the nicotinic synaptic mechanisms in midbrain dopaminergic areas. In summary, nicotine as obtained from tobacco interacts with multiple nicotinic acetylcholine receptor subtypes on dopamine, GABA, glutaminergic neuron to produce not only the acute positive reinforcement but also the synaptic changes associated with learning and memory.
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