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Titolo:
CHOLECYSTOKININ AND NEUROTENSIN INVERSELY MODULATE EXCITATORY SYNAPTIC TRANSMISSION IN THE PARABRACHIAL NUCLEUS IN-VITRO
Autore:
SALEH TM; KOMBIAN SB; ZIDICHOUSKI JA; PITTMAN QJ;
Indirizzi:
UNIV CALGARY,NEUROSCI RES GRP CALGARY AB CANADA UNIV CALGARY,NEUROSCI RES GRP CALGARY AB CANADA CIBA GEIGY LTD CALGARY AB T2N 4N1 CANADA
Titolo Testata:
Neuroscience
fascicolo: 1, volume: 77, anno: 1997,
pagine: 23 - 35
SICI:
0306-4522(1997)77:1<23:CANIME>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPUS; VISCERAL INPUT; CCK RECEPTORS; SUDDEN-DEATH; NEURONS; INHIBITION; BRAIN; LOCALIZATION; ANTAGONIST; RECORDINGS;
Keywords:
VISCERAL AFFERENT; SR48692; L-365,260; L-364,718; PAIRED-PULSE DEPRESSION; PRESYNAPTIC INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
T.M. Saleh et al., "CHOLECYSTOKININ AND NEUROTENSIN INVERSELY MODULATE EXCITATORY SYNAPTIC TRANSMISSION IN THE PARABRACHIAL NUCLEUS IN-VITRO", Neuroscience, 77(1), 1997, pp. 23-35

Abstract

Cholecystokinin and neurotensin are present in fibres innervating theparabrachial nucleus and have previously been shown to modulate the flow of visceral afferent information through the parabrachial nucleus to the cortex in the rat. This study examined the effects of cholecystokinin and neurotensin on synaptic transmission in the parabrachial nucleus using a pontine slice preparation and the nystatin perforated-patch recording technique. Stimulation of the ventral, external lateral portion of the parabrachial nucleus elicited glutamate-mediated, excitatory postsynaptic currents in cells recorded in the parabrachial nucleus. Bath application of neurotensin dose-dependently and reversibly enhanced, while cholecystokinin attenuated, the evoked excitatory postsynaptic current. In addition, the frequency of spontaneous, miniature excitatory postsynaptic currents recorded in parabrachial nucleus cells was significantly increased by neurotensin and decreased by cholecystokinin application. Paired-pulse depression was also enhanced and decreased by neurotensin and cholecystokinin, respectively. These synaptic changes induced by neurotensin and cholecystokinin were not accompanied by changes in input resistance of parabrachial nucleus cells over a wide voltage range (although neurotensin reduced an outwardly rectifying conductance at potentials positive to - 20 mV), nor did these peptides alter the inward current induced by a brief bath application of the glutamate agonist, lpha-amino-3-hydroxy-methylisoxazole-4-propionate. The neurotensin antagonist, SR48692 (100 mu M), completely and reversibly blocked the neurotensin-induced enhancement of the excitatory postsynaptic current. The non-selective cholecystokinin receptor antagonist, proglumide (100 mu M), completely and reversibly blocked the cholecystokinin-induced attenuation of the excitatory postsynaptic current. In addition, the selective cholecystokinin-A receptor antagonist, L-364,718 (10 mu M), but not the selective cholecystokinin-B receptor antagonist, L-365,260 (100 mu M), blocked the effect of cholecystokinin on synaptic transmission. These results suggest that neurotensin andcholecystokinin act at presynaptic neurotensin and cholecystokinin-A receptors, respectively, to modulate excitatory synaptic transmission in the parabrachial nucleus. Copyright (C) 1997 IBRO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:40:46