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The Journal of Neuroscience, March 1, 1998, 18(5):1904-1912

Presynaptic Nicotinic Receptors Facilitate Monoaminergic Transmission

Xiangyang Li, Donald G. Rainnie, Robert W. McCarley, and Robert W. Greene

Harvard Medical School and Brockton Veterans Administration Medical Center, Neuroscience Laboratory, Brockton, Massachusetts 02401

Nicotine is reported to increase arousal and attention and to elevate mood, effects that are most often associated with changes in the function of monoaminergic neuromodulatory systems (). Recent studies have shown a nicotinic receptor-mediated presynaptic enhancement of fast glutamatergic (; ) and GABAergic () transmission. However, the mechanism of nicotinic effects on metabotropic-mediated transmission in general, and on monoaminergic transmission in particular, is less well understood. We have examined nicotinic effects on dorsal raphe neurons of rats using whole-cell current and voltage-clamp recording techniques in vitro. In the majority of these neurons, activation of presynaptic nicotinic receptors induced a depolarization mediated by norepinephrine acting on alpha 1 receptors. Blockade of this response revealed a hyperpolarization mediated by serotonin acting on 5-HT1A receptors. Because the norepinephrine effect was sensitive to methyllycaconitine (100 nM), it is concluded that nicotinic receptors with an alpha 7 subunit can facilitate release of norepinephrine to activate metabotropic receptors. In contrast, methyllycaconitine-insensitive nicotinic receptors can induce 5-HT release in the dorsal raphe nucleus.

Key words: norepinephrine; serotonin; acetylcholine; methyllycaconitine; dorsal raphe; electrophysiology


Copyright © 1998 Society for Neuroscience  0270-6474/98/1851904-09$05.00/0


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