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Titolo:
Basal forebrain glutamatergic modulation of cortical acetylcholine release
Autore:
Fadel, J; Sarter, M; Bruno, JP;
Indirizzi:
Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA Ohio State Univ Columbus OH USA 43210 ept Psychol, Columbus, OH 43210 USA Ohio State Univ, Dept Neurosci, Columbus, OH 43210 USA Ohio State Univ Columbus OH USA 43210 pt Neurosci, Columbus, OH 43210 USA
Titolo Testata:
SYNAPSE
fascicolo: 3, volume: 39, anno: 2001,
pagine: 201 - 212
SICI:
0887-4476(20010301)39:3<201:BFGMOC>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
BENZODIAZEPINE RECEPTOR LIGANDS; CHOLINERGIC NEURONS; NUCLEUS BASALIS; ELECTROENCEPHALOGRAM DESYNCHRONIZATION; BIDIRECTIONAL MODULATION; FRONTOPARIETAL CORTEX; CEREBRAL-CORTEX; RAT-BRAIN; IN-VIVO; MICRODIALYSIS;
Keywords:
acetylcholine; basal forebrain; cortex; microdialysis; glutamate receptors; kainate; NMDA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Bruno, JP Ohio State Univ, Dept Psychol, 31 Townshend Hall, Columbus, OH 43210 USA Ohio State Univ 31 Townshend Hall Columbus OH USA 43210 3210 USA
Citazione:
J. Fadel et al., "Basal forebrain glutamatergic modulation of cortical acetylcholine release", SYNAPSE, 39(3), 2001, pp. 201-212

Abstract

The mediation of cortical ACh release by basal forebrain glutamate receptors was studied in awake rats fitted with microdialysis probes in medial prefrontal cortex and ipsilateral basal forebrain. Repeated presentation of a stimulus consisting of exposure to darkness with the opportunity to consumea sweetened cereal resulted in a transient increase in cortical ACh efflux. This stimulated release was dependent on basal forebrain glutamate receptor activity as intrabasalis perfusion with the ionotropic glutamate receptor antagonist kynurenate (1.0 mM) markedly attenuated darkness/cereal-induced ACh release. Activation of AMPA/kainate receptors by intrabasalis perfusion of kainate (100 muM) was sufficient to increase cortical ACh efflux evenunder basal (nonstimulated) conditions. This effect of kainate was blockedby coperfusion with the antagonist DNQX (0.1-5.0 mM). Stimulation of NMDA receptors with intrabasalis perfusion of NMDA (50 or 200 muM) did not increase basal cortical ACh efflux. However, perfusion of NMDA in rats followingexposure to the darkness/cereal stimulus resulted in a potentiation of both the magnitude and duration of stimulated cortical ACh efflux. Moreover, intrabasalis perfusion of the higher dose of NMDA resulted in a rapid increase in cortical ACh efflux even before presentation of the darkness/cereal. stimulus, suggesting an anticipatory change in the excitability of basal forebrain cholinergic neurons. These data demonstrate that basal forebrain glutamate receptors contribute to the stimulation of cortical ACh efflux in response to behavioral stimuli. The specific roles of basal forebrain glutamate receptor subtypes in mediating cortical ACh release differ and depend on the level of activity of basal forebrain cholinergic neurons. (C) 2001 Wiley-Liss, Inc.

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Documento generato il 05/04/20 alle ore 04:34:55