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Titolo:
CALCITONIN GENE-RELATED PEPTIDE POTENTIATES SYNAPTIC RESPONSES AT DEVELOPING NEUROMUSCULAR-JUNCTION
Autore:
LU B; FU WM; GREENGARD P; POO MM;
Indirizzi:
ROCKEFELLER UNIV,MOLEC & CELLULAR NEUROSCI LAB NEW YORK NY 10021 COLUMBIA UNIV,DEPT BIOL SCI NEW YORK NY 10027
Titolo Testata:
Nature
fascicolo: 6424, volume: 363, anno: 1993,
pagine: 76 - 79
SICI:
0028-0836(1993)363:6424<76:CGPPSR>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
NICOTINIC ACETYLCHOLINE-RECEPTOR; CHICK SKELETAL-MUSCLE; EMBRYONIC NEURON; RAPID INDUCTION; INITIAL EVENTS; SPINAL-CORD; PHOSPHORYLATION; MYOTUBES; DESENSITIZATION; CULTURE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
B. Lu et al., "CALCITONIN GENE-RELATED PEPTIDE POTENTIATES SYNAPTIC RESPONSES AT DEVELOPING NEUROMUSCULAR-JUNCTION", Nature, 363(6424), 1993, pp. 76-79

Abstract

PROTEIN phosphorylation is important in synaptic transmission and plasticity1. At the neuromuscular junction, phosphorylation of acetylcholine (ACh) receptor-channels increases the rate of agonist-induced channel desensitization2. In contrast, potentiation of ACh channel activity through protein phosphorylation has not been described. We report here that calcitonin gene-related peptide (CGRP), a neuropeptide presentat presynaptic motor nerve terminals3,4, enhances the postsynaptic response at developing neuromuscular junctions by increasing the burst duration of embryonic ACh channels. The effect of CGRP on these ACh channels is mimicked by dibutyryl-cyclic AMP and by cAMP-dependent protein kinase (PKA) and prevented by a specific peptide inhibitor of PKA. Moreover, postsynaptic inhibition of PKA reduced the amplitude and decay time of spontaneous synaptic currents, suggesting that endogenous CGRP may act as a potentiating factor during the early phase of synaptogenesis.

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Documento generato il 02/04/20 alle ore 02:33:02