Linked Life Data

7683114

Source:http://linkedlifedata.com/resource/pubmed/id/7683114

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6424
pubmed:dateCreated
1993-5-27
pubmed:abstractText
Protein phosphorylation is important in synaptic transmission and plasticity. At the neuromuscular junction, phosphorylation of acetylcholine (ACh) receptor-channels increases the rate of agonist-induced channel desensitization. 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 present at presynaptic motor nerve terminals, 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
363
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
76-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Calcitonin gene-related peptide potentiates synaptic responses at developing neuromuscular junction.
pubmed:affiliation
Laboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, New York 10021.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.