Opioid receptor modulation of a metabolically sensitive ion channel in ratamygdala neurons

Citation
Xg. Chen et al., Opioid receptor modulation of a metabolically sensitive ion channel in ratamygdala neurons, J NEUROSC, 21(23), 2001, pp. 9092-9100
Citations number
45
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE
ISSN journal
0270-6474 → ACNP
Volume
21
Issue
23
Year of publication
2001
Pages
9092 - 9100
Database
ISI
SICI code
0270-6474(200112)21:23<9092:ORMOAM>2.0.ZU;2-C
Abstract
We have used single-channel patch-clamp recordings to study opiate receptor effects on freshly dissociated neurons from the rat amygdalohippocampal ar ea (also called the posterior nucleus of the amygdala), an output nucleus o f the amygdala implicated in appetitive behaviors. Dissociated cells includ ed a distinct subpopulation that was 30-40 mum in diameter, multipolar or p yramidal in shape, and immunoreactive for neuron-specific enolase, mu opioi d receptors, and galanin. In whole-cell perforated-patch recordings, these cells responded to low concentrations of mu opioid agonists with a hyperpol arization. In cell-attached single channel recordings, these cells expresse d a large variety of K+-permeable ion channels, including 20-100 pS inward rectifiers and 150-200 pS apparent Ca2+-activated K+ channels, none of whic h appeared sensitive to the presence of opioid drugs. In contrast, a 130 pS inwardly rectifying channel was selectively activated by mu opioid recepto rs in this same subpopulation of cells and was active only in the presence of opioid agonists, and inhibited in the presence of antagonists. Channels identical to the 130 pS channel in conductance and voltage sensitivity were activated in the absence of opioids, when the cells were treated with gluc ose-free medium or with the metabolic inhibitor rotenone. The sulfonylurea drug tolbutamide inhibited 130 pS channel openings elicited by opioids. Thu s, a subpopulation of amygdala projection neurons expresses a metabolically sensitive ion channel that is selectively modulated by opiate receptors. T his mechanism may allow opioid neurotransmitters to regulate ingestive beha viors, and thus, opiate drugs to influence reward pathways.