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

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 nicotin...

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Bibliographic Details
Published in:The Journal of neuroscience 2009-08, Vol.29 (33), p.10436-10448
Main Authors: Tu, Bin, Gu, Zhenglin, Shen, Jian-xin, Lamb, Patricia W, Yakel, Jerrel L
Format: Article
Language:English
Subjects:
Animals
Entorhinal Cortex - drug effects
Entorhinal Cortex - physiology
In Vitro Techniques
Membrane Potentials - drug effects
Membrane Potentials - physiology
Neurons - drug effects
Neurons - physiology
Nicotine - pharmacology
Rats
Rats, Wistar
Synaptic Transmission - drug effects
Synaptic Transmission - physiology
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Summary: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-alpha7 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 alpha7 and non-alpha7 subtypes of nAChRs. Our data suggest that ECVI neurons are important regulators of hippocampal function and plasticity during smoking.
ISSN:0270-6474
1529-2401
DOI:10.1523/JNEUROSCI.2580-09.2009