EXTRANUCLEAR DENDRITES OF LOCUS-COERULEUS NEURONS - ACTIVATION BY GLUTAMATE AND MODULATION OF ACTIVITY BY ALPHA-ADRENOCEPTORS

Citation
A. Ivanov et G. Astonjones, EXTRANUCLEAR DENDRITES OF LOCUS-COERULEUS NEURONS - ACTIVATION BY GLUTAMATE AND MODULATION OF ACTIVITY BY ALPHA-ADRENOCEPTORS, Journal of neurophysiology, 74(6), 1995, pp. 2427-2436
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences,Physiology,Neurosciences,Physiology
Journal title
ISSN journal
0022-3077
Volume
74
Issue
6
Year of publication
1995
Pages
2427 - 2436
Database
ISI
SICI code
0022-3077(1995)74:6<2427:EDOLN->2.0.ZU;2-J
Abstract
1. Locus coeruleus (LC) neurons were recorded extracellularly and intr acellularly in rat brain slices. Effects of glutamate applied to the a rea of distal extranuclear LC dendrites, and of alpha-2 adrenoceptors applied in the bath, were determined on activity of these cells. 2. Gl utamate applied to the area of distal dendrites potently activated LC neurons. These responses were not blocked by either 1 mu M tetrodotoxi n or 2 mM Co2+ -10 mM Mg2+. This indicates that glutamate acting direc tly on distal dendrites can potently activate LC neurons. 3. Bath appl ication of the alpha-2 adrenoceptor antagonists yohimbine (1 mu M) or idazoxan (1 mu M) significantly increased responses of LC neurons evok ed by dendritic glutamate application. These antagonist treatments als o transiently decreased, and then increased, spontaneous discharge act ivity in LC neurons.4. Alterations in spontaneous and glutamate-evoked activities after blockade of alpha-2 adrenoreceptors were not observe d in LC neurons of reserpinized rats. This indicates that the altered LC activity and responsiveness to glutamate following alpha-2 antagoni st treatment in nonreserpinized slices are mediated via blockade of ef fects of endogenously released noradrenaline. 5. The alpha-1 antagonis t prazosin (1 mu M) caused a small but reliable decrease in the sponta neous firing rate of LC neurons. After prazosin pretreatment, alpha-2 antagonists did not evoke the expected delayed increase in LC spontane ous firing and response to glutamate application. These results indica te that activation of alpha-1 adrenoceptors may contribute to the dela yed increase in excitability of LC neurons after alpha-2 antagonist ad ministration. The possible roles of alpha-1 and alpha-2 adrenoreceptor s in regulation of spontaneous discharge rate and glutamate-evoked res ponses in LC neurons are discussed.