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Cerebral Cortex Advance Access originally published online on September 15, 2008
Cerebral Cortex 2009 19(5):1079-1091; doi:10.1093/cercor/bhn158
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Functional Expression of Nicotinic Acetylcholine Receptors in Rat Neocortical Layer 5 Pyramidal Cells

Gerd Zolles1, Eva Wagner, Angelika Lampert and Bernd Sutor

Institute of Physiology, Department of Physiological Genomics, Ludwig-Maximilians-University of Munich, Schillerstrasse 46, 80336 Munich, Germany

Address correspondence to Dr Bernd Sutor, Institute of Physiology, Department of Physiological Genomics, Ludwig-Maximilians-University of Munich, Schillerstrasse 46, 80336 Munich, Germany. Email: bernd.sutor{at}lrz.uni-muenchen.de.

Neuronal nicotinic acetylcholine receptors (nAChRs) expressed by neurons of the neocortex are known to play a role in higher brain functions. Electrophysiological studies of neocortical neurons provided evidence that functional nAChRs are present on the axonal presynaptic terminals, on the somata and on dendrites of gamma-aminobutyric acid (GABA)ergic inhibitory interneurons. However, it is not clear if pyramidal neurons express functional postsynaptic nAChRs. Therefore, we investigated the action of locally applied acetylcholine (ACh) on layer 5 pyramidal neurons in the rat neocortex in vitro. In the presence of atropine, tetrodotoxin, glutamate receptor antagonists, and GABAA receptor antagonists, ACh induced membrane depolarizations which were generated by membrane inward currents consisting of a fast and a slow component. Analysis of the electrophysiological properties, the pharmacological characteristics, and the desensitization behavior of the 2 current components revealed that they were mediated by at least 2 different subtypes of the nAChR, most likely the {alpha}7-like and the {alpha}4β2-like subtype. The expression of nAChRs in neocortical pyramidal cells raises the possibility that these neurons generate nicotinic excitatory postsynaptic potentials, thereby influencing cell excitability. Furthermore, because most nAChRs are permeable to calcium, they may modulate synaptic transmission and neuronal plasticity via a calcium-dependent postsynaptic mechanism.

Key Words: layer 5 • neocortex • nicotinic acetylcholine receptors • postsynaptic membrane currents • pyramidal cells

1 Present address: Department of Physiology II, Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Strasse 7, 79104 Freiburg, Germany.


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