Abstract
Homeostatic signaling systems are thought to interface with the mechanisms of neural plasticity to achieve stable yet flexible neural circuitry. However, the time course, molecular design, and implementation of homeostatic signaling remain poorly defined. Here we demonstrate that a homeostatic increase in presynaptic neurotransmitter release can be induced within minutes following postsynaptic glutamate receptor blockade. The rapid induction of synaptic homeostasis is independent of new protein synthesis and does not require evoked neurotransmission, indicating that a change in the efficacy of spontaneous quantal release events is sufficient to trigger the induction of synaptic homeostasis. Finally, both the rapid induction and the sustained expression of synaptic homeostasis are blocked by mutations that disrupt the pore-forming subunit of the presynaptic Ca(V)2.1 calcium channel encoded by cacophony. These data confirm the presynaptic expression of synaptic homeostasis and implicate presynaptic Ca(V)2.1 in a homeostatic retrograde signaling system.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Calcium Channels / genetics
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Calcium Channels / metabolism*
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Calcium Channels, N-Type / genetics
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Calcium Channels, N-Type / metabolism*
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Drosophila Proteins / genetics
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Drosophila Proteins / metabolism*
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Drosophila melanogaster / genetics
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Drosophila melanogaster / metabolism*
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Excitatory Postsynaptic Potentials / drug effects
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Excitatory Postsynaptic Potentials / physiology
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Homeostasis / genetics*
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Membrane Potentials / drug effects
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Membrane Potentials / genetics
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Motor Neurons / drug effects
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Motor Neurons / metabolism
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Mutation / genetics
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Neuromuscular Junction / drug effects
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Neuromuscular Junction / genetics
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Neuromuscular Junction / metabolism*
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Receptors, AMPA / antagonists & inhibitors
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Receptors, AMPA / genetics
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Receptors, AMPA / metabolism
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Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
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Receptors, N-Methyl-D-Aspartate / genetics
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Receptors, N-Methyl-D-Aspartate / metabolism
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Synaptic Membranes / drug effects
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Synaptic Membranes / genetics
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Synaptic Membranes / metabolism
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Synaptic Transmission / drug effects
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Synaptic Transmission / genetics*
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Synaptic Vesicles / drug effects
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Synaptic Vesicles / metabolism
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Time Factors
Substances
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Calcium Channels
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Calcium Channels, N-Type
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Drosophila Proteins
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Receptors, AMPA
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Receptors, N-Methyl-D-Aspartate
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cac protein, Drosophila
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voltage-dependent calcium channel (P-Q type)
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glutamate receptor ionotropic, AMPA 2