期刊
SCIENCE
卷 310, 期 5749, 页码 858-863出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1117541
关键词
-
资金
- NINDS NIH HHS [R01 NS040296-06, R01 NS043244, R01 NS040296] Funding Source: Medline
The molecular pathways involved in retrograde signal transduction at synapses and the function of retrograde communication are poorly understood. Here, we demonstrate that postsynaptic calcium 2+ ion (Ca2+) influx through glutamate receptors and subsequent postsynaptic vesicle fusion trigger a robust induction of presynaptic miniature release after high-frequency stimulation at Drosophila neuromuscular. junctions. An isoform of the synaptotagmin family, synaptotagmin 4 (Syt 4), serves as a postsynaptic Ca2+ sensor to release retrograde signals that stimulate enhanced presynaptic function through activation of the cyclic adenosine monophosphate (cAMP)-cAMP-dependent protein kinase pathway. Postsynaptic Ca2+ influx also stimulates local synaptic differentiation and growth through Syt 4-mediated retrograde signals in a synapse-, specific manner.
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