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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 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 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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