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The Journal of Neurophysiology Vol. 87 No. 3 March 2002, pp. 1651-1654
Copyright ©2002 by the American Physiological Society
RAPID COMMUNICATION
7 Nicotinic Acetylcholine Receptor Modulates Excitatory
Input to Hippocampal CA1 Interneurons
1Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, Maryland 21201; and 2Departamento de Farmacologia Básica e Clínica, Instituto de Ciências Biomédicas, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21944, Brazil
Alkondon, Manickavasagom and
Edson X. Albuquerque.
A Non-7 Nicotinic Acetylcholine Receptor Modulates Excitatory
Input to Hippocampal CA1 Interneurons. J. Neurophysiol. 87: 1651-1654, 2002. The nicotinic
acetylcholine receptor (nAChR), particularly the 
7 subtype, has
received profound attention for its role in modifying excitatory
postsynaptic currents (EPSCs) in hippocampal pyramidal neurons as well
as in neurons from other brain regions. Here, we tested the possibility
that an nAChR could affect EPSCs in the interneurons of rat hippocampal
slices. Using whole-cell patch-clamp technique on CA1 stratum radiatum
interneurons and U-tube application of agents, we show that nicotinic
agonists enhance EPSC frequency in interneurons. Among the agents
tested, cytisine and mecamylamine were the most effective agonist and antagonist, respectively, suggesting a role for 3
4-containing nAChRs in the modulation of interneuron EPSCs. Ligands selective for
the 7 nAChR had very little or no effect on interneuron EPSCs. Low
concentrations of nicotine also enhanced EPSC frequency, implicating the involvement of non-7 nAChRs in controlling interneuron
excitability in smokers. We conclude that nAChR-dependent EPSC
modulation in the hippocampus is both subtype- and neuron-specific and
that a non-7 nAChR, presumably 34, controls glutamate
transmission to CA1 interneurons.
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