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Titolo:
A presynaptic mechanism contributes to depression of autonomic signal transmission in NTS
Autore:
Chen, CY; Horowitz, JM; Bonham, AC;
Indirizzi:
Univ Calif Davis, Div Cardiovasc Med, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 v Cardiovasc Med, Davis, CA 95616 USA Univ Calif Davis, Dept Pharmacol, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 , Dept Pharmacol, Davis, CA 95616 USA Univ Calif Davis, Dept Neurobiol Physiol & Behav, Davis, CA 95616 USA UnivCalif Davis Davis CA USA 95616 Physiol & Behav, Davis, CA 95616 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 4, volume: 277, anno: 1999,
pagine: H1350 - H1360
SICI:
0363-6135(199910)277:4<H1350:APMCTD>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEUS-TRACTUS-SOLITARIUS; METABOTROPIC GLUTAMATE RECEPTORS; SYNAPTIC TRANSMISSION; NEUROTRANSMITTER RELEASE; TERM POTENTIATION; NMDA RECEPTORS; AMPA RECEPTORS; RAT; NEURONS; INVITRO;
Keywords:
voltage-clamp; excitatory postsynaptic currents; alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid; N-methyl-D-aspartic acid; short-term plasticity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Bonham, AC Univ Calif Davis, Div Cardiovasc Med, TB 172 1 Shields Ave, Davis, CA 95616 USA Univ Calif Davis TB 172 1 Shields Ave Davis CA USA 95616 16 USA
Citazione:
C.Y. Chen et al., "A presynaptic mechanism contributes to depression of autonomic signal transmission in NTS", AM J P-HEAR, 277(4), 1999, pp. H1350-H1360

Abstract

With increasing frequencies of autonomic afferent input to the nucleus tractus solitarii (NTS), postsynaptic responses are depressed. To test the hypothesis that a presynaptic mechanism contributes to this frequency-dependent depression, me used whole cell, voltage-clamp recordings in an NTS slice. First, we determined whether solitary tract stimulation (0.4-24 Hz) resulted in frequency-dependent depression of excitatory postsynaptic currents (EPSCs) in second-order neurons. Second, because decreases in presynaptic glutamate release result in a parallel depression of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor-mediated components of EPSCs, we determined whether the magnitude,time course, and recovery from the depression were the same in both EPSC components. Third, to determine whether AMPA receptor desensitization contributed, we examined the depression during cyclothiazide. EPSCs decreased in a frequency-dependent manner by up to 76% in second- and 92% in higher-order neurons. AMPA and NMDA EPSC components were depressed with the same magnitude (by 83% and 83%) and time constant (113 and 103 ms). The time constantfor the recovery was also not different (1.2 and 0.8 s). Cyclothiazide didnot affect synaptic depression at greater than or equal to 3 Hz. The data suggest that presynaptic mechanism(s) at the first NTS synapse mediate frequency-dependent synaptic depression.

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Documento generato il 02/07/20 alle ore 18:33:51