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Vol. 283, Issue 2, 675-683, 1997
3, 4, and 7 Neuronal Nicotinic Receptor
Subtypes1
Department of Biology, University of Pennsylvania. (F.O.),
and
Department of Neuroscience, University of Pennsylvania Medical
School, Philadelphia, Pennsylvania (V.G., A.K., F.W., J.L.)
Because chronic exposure to nicotine and nicotinic drugs might both
activate and desensitize nicotinic acetylcholine receptors (AChRs), we
sought to determine whether prolonged exposure to nicotine
concentrations encountered in tobacco users differentially affects
electrophysiological properties of major subtypes of human neuronal
nicotinic AChRs. Xenopus laevis oocytes were injected with subunit cRNAs encoding (1) homomeric 
7 AChRs, (2) heteromeric 4
2 AChRs and (3) heteromeric 3 AChRs formed from combinations of 3, 2, 4 and 5 cRNAs. Acute activation required
micromolar concentrations of nicotine. Chronic exposure to
submicromolar concentrations of nicotine irreversibly inactivated many
42 AChRs and 7 AChRs but inhibited 3 AChRs much less. Thus,
although 3 AChRs are present in the brain in much smaller amounts
than are 42 AChRs or 7 AChRs, 3 AChRs in brain and
autonomic ganglia may be able to play a relatively large role in acute
responses to endogenous ACh or subsequent doses of nicotine after
chronic exposure to nicotine. The behavioral effects of nicotine may
typically reflect the sustained inhibition of 42 AChRs and 7
AChRs in combination with the residual susceptibility of 3 AChRs and
perhaps some other AChR subtypes for acute activation. Tolerance for
nicotine exhibited by tobacco users may reflect the long-term
irreversible functional inactivation of 42 AChRs and 7 AChRs
produced by chronic exposure to nicotine.
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