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Cholinergic modulation of nucleus accumbens medium spiny neurons
Author(s) -
De Rover Mischa,
Lodder Johannes C.,
Kits Karel S.,
Schoffelmeer Anton N. M.,
Brussaard Arjen B.
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02289.x
Subject(s) - nicotinic agonist , nucleus accumbens , acetylcholine , cholinergic , muscarinic acetylcholine receptor , neuroscience , medium spiny neuron , chemistry , acetylcholine receptor , cholinergic neuron , glutamatergic , biology , receptor , endocrinology , central nervous system , glutamate receptor , biochemistry , basal ganglia
The rat nucleus accumbens contains acetylcholine‐releasing interneurons, presumed to play a regulatory role in the electrical activity of medium spiny output neurons. In order to examine this issue in detail, we made electrophysiological recordings in rat nucleus accumbens slices. These experiments showed that γ‐aminobutyric acid‐mediated inhibition of the output neurons might be facilitated by activation of nicotinic acetylcholine receptors, in addition to being suppressed via activation of muscarinic acetylcholine receptors. In contrast, glutamatergic excitation of output neurons appeared to be inhibited by activation of muscarinic acetylcholine receptors and to be insensitive to activation of nicotinic acetylcholine receptors. The spontaneous firing frequency of cholinergic neurons appeared to be under control of both a muscarinic and a nicotinic pathway in a bi‐directional manner. Finally, we made paired recordings in which the functional connection between cholinergic neurons and output neurons was monitored. Driving the cholinergic neurons at physiological firing frequencies stimulated γ‐aminobutyric acid‐mediated inhibition of the output neurons, via activation of nicotinic acetylcholine receptors. The onset of this effect was slow and lacked a fixed delay. These data indicate that activation of nicotinic acetylcholine receptors in rat nucleus accumbens may mediate the facilitation of γ‐aminobutyric acid‐mediated inhibition of medium spiny output neurons. Possible mechanisms of neurotransmission, mediating this cholinergic modulation are discussed.