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Vol. 289, Issue 2, 656-660, May 1999
Department of Physiology, University of Arizona College of
Medicine, Tucson, Arizona
When subjected to prolonged exposure to nicotinic agonists, nicotinic
acetylcholine receptors undergo desensitization, resulting in an
inactive receptor that does not allow for the passage of ions. The
induction of desensitization of diverse nicotinic acetylcholine receptor subtypes in muscle, ganglia, or brain is likely to play important modulatory roles in synaptic transmission. Furthermore, nicotinic receptor desensitization may contribute to behavioral changes
in humans or animals subjected to prolonged nicotine exposure pharmacologically or through the use of tobacco products. We
investigated the recovery from desensitization of muscle-type nicotinic
acetylcholine receptors in TE671/RD cells induced by exposure to
acetylcholine or nicotine. Rates of recovery from desensitization are
dependent on the length of agonist exposure and on the agonist used to
induce desensitization. Increasing the time of exposure results in an increase in the time constant of recovery for both agonists. The recovery from nicotine-induced desensitization is consistently faster
than the recovery from acetylcholine-induced desensitization regardless
of whether nicotine or acetylcholine is used to assess levels of
desensitization. These findings suggest the existence of more than one
state of receptor desensitization and that nicotinic agonists vary in
their efficiency of inducing receptors to states of differing depths of desensitization.
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