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J Neurophysiol 87: 1651-1654, 2002;
0022-3077/02 $5.00
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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

A Non-alpha 7 Nicotinic Acetylcholine Receptor Modulates Excitatory Input to Hippocampal CA1 Interneurons

Manickavasagom Alkondon1 and Edson X. Albuquerque1,2

 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-alpha 7 Nicotinic Acetylcholine Receptor Modulates Excitatory Input to Hippocampal CA1 Interneurons. J. Neurophysiol. 87: 1651-1654, 2002. The nicotinic acetylcholine receptor (nAChR), particularly the alpha 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 alpha 3beta 4-containing nAChRs in the modulation of interneuron EPSCs. Ligands selective for the alpha 7 nAChR had very little or no effect on interneuron EPSCs. Low concentrations of nicotine also enhanced EPSC frequency, implicating the involvement of non-alpha 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-alpha 7 nAChR, presumably alpha 3beta 4, controls glutamate transmission to CA1 interneurons.




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