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The Journal of Neuroscience, August 19, 2009, 29(33):10436-10448; doi:10.1523/JNEUROSCI.2580-09.2009

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Cellular/Molecular
Characterization of a Nicotine-Sensitive Neuronal Population in Rat Entorhinal Cortex

Bin Tu, Zhenglin Gu, Jian-xin Shen, Patricia W. Lamb, and Jerrel L. Yakel

Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709

Correspondence should be addressed to Jerrel L. Yakel, National Institute of Environmental Health Sciences, F2-08, P.O. Box 12233, 111 T. W. Alexander Drive, Research Triangle Park, NC 27709. Email: yakel{at}niehs.nih.gov

The entorhinal cortex (EC) is a part of the hippocampal complex that is essential to learning and memory, and nicotine affects memory by activating nicotinic acetylcholine receptors (nAChRs) in the hippocampal complex. However, it is not clear what types of neurons in the EC are sensitive to nicotine and whether they play a role in nicotine-induced memory functions. Here, we have used voltage-sensitive dye imaging methods to locate the neuronal populations responsive to nicotine in entorhino-hippocampal slices and to clarify which nAChR subtypes are involved. In combination with patch-clamp methods, we found that a concentration of nicotine comparable to exposure during smoking depolarized neurons in layer VI of the EC (ECVI) by acting through the non-7 subtype of nAChRs. Neurons in the subiculum (Sb; close to the deep EC layers) also contain nicotine-sensitive neurons, and it is known that Sb neurons project to the ECVI. When we recorded evoked EPSCs (eEPSCs) from ECVI neurons while stimulating the Sb near the CA1 region, a low dose of nicotine not only enhanced synaptic transmission (by increasing eEPSC amplitude) but also enhanced plasticity by converting tetanus stimulation-induced short-term potentiation to long-term potentiation; nicotine enhanced synaptic transmission and plasticity of ECVI synapses by acting on both the 7 and non-7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.

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Received June 2, 2009; revised July 20, 2009; accepted July 22, 2009.

Correspondence should be addressed to Jerrel L. Yakel, National Institute of Environmental Health Sciences, F2-08, P.O. Box 12233, 111 T. W. Alexander Drive, Research Triangle Park, NC 27709. Email: yakel{at}niehs.nih.gov

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