Abstract
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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Animals, Genetically Modified
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Calcium / metabolism
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Cell Differentiation / genetics
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Cell Differentiation / physiology
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Cyclic AMP / metabolism
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Cyclic AMP-Dependent Protein Kinases / metabolism
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Drosophila / embryology
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Drosophila / growth & development
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Drosophila / physiology*
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Egtazic Acid / analogs & derivatives
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Egtazic Acid / pharmacology
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Embryo, Nonmammalian / cytology
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Embryo, Nonmammalian / physiology
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Excitatory Postsynaptic Potentials
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Feedback, Physiological
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Models, Neurological
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Mutation
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Neuromuscular Junction / physiology*
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Neuronal Plasticity
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Presynaptic Terminals / physiology
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Receptors, Glutamate / metabolism
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Signal Transduction*
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Synapses / physiology*
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Synapses / ultrastructure
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Synaptic Membranes / physiology
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Synaptic Transmission
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Synaptic Vesicles / physiology
Substances
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Receptors, Glutamate
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Egtazic Acid
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Cyclic AMP
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Cyclic AMP-Dependent Protein Kinases
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1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
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Calcium