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Titolo:
BDNF-dependent enhancement of exocytosis in cultured cortical neurons requires translation but not transcription
Autore:
Bradley, J; Sporns, O;
Indirizzi:
Inst Neurosci, San Diego, CA 92121 USA Inst Neurosci San Diego CA USA 92121 st Neurosci, San Diego, CA 92121 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1, volume: 815, anno: 1999,
pagine: 140 - 149
SICI:
0006-8993(19990102)815:1<140:BEOEIC>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDIVIDUAL HIPPOCAMPAL SYNAPSES; LOCAL PROTEIN-SYNTHESIS; LONG-TERM POTENTIATION; MOTOR-NERVE TERMINALS; RAT VISUAL-CORTEX; NEUROTROPHIC FACTOR; SYNAPTIC TRANSMISSION; SIGNAL-TRANSDUCTION; GROWTH-FACTOR; RELEASE;
Keywords:
brain-derived neurotrophic factor; exocytosis; synaptic vesicle; FMI-43; neurotransmitter; synaptic plasticity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Sporns, O Inst Neurosci, 10640 John Jay Hopkins Dr, San Diego, CA 92121 USA Inst Neurosci 10640 John Jay Hopkins Dr San Diego CA USA 92121 A
Citazione:
J. Bradley e O. Sporns, "BDNF-dependent enhancement of exocytosis in cultured cortical neurons requires translation but not transcription", BRAIN RES, 815(1), 1999, pp. 140-149

Abstract

Neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), are involved in acute modulation of synaptic plasticity. Different modes of action of BDNF have been described with time courses ranging from seconds tohours, but the sequence of cellular processes responsible for BDNF-dependent modulation of synaptic plasticity is unknown. We have used optical imaging of the styryl dye, FM1-43, which selectively labels synaptic vesicles, to investigate potential presynaptic effects of BDNF. Addition of BDNF to cultured cortical neurons for 3 h produced a significant enhancement of exocytosis upon modest depolarization. BDNF had no effect on exocytosis either immediately or after incubation for 30 min. BDNF-dependent enhancement of exocytosis was blocked by the tyrosine kinase inhibitor, K252a, but not by K252b, consistent with signalling via the TrkB receptor. Having demonstrated that the BDNF-dependent enhancement of synaptic vesicle release was presentonly after 1 h, we investigated whether de novo gene transcription and/or protein synthesis were involved. Addition of the inhibitors of RNA synthesis, actinomycin D, or 5,6-dichloro-1-beta-D-ribofuranosyl benzimidazole (DRB), did not affect the enhancement of exocytosis produced by BDNF. However, the effect of BDNF was blocked by the inhibitors of translation, cycloheximide or anisomycin. Our results indicate a rapid BDNF-dependent enhancement of neurotransmitter release that requires translation but not transcription. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 19:14:35