A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

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Citation Frank, C.A., Kennedy, M.J., Goold, C.P., Marek, K.W., Davis, G.W. (2006). Mechanisms underlying the rapid induction and sustained expression of synaptic homeostasis.  Neuron 52(4): 663--677. (Export to RIS)
FlyBase ID FBrf0209547
Publication Type Research paper
PubMed ID 17114050
PubMed 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.
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Language of Publication English
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Publication Type Journal
Abbreviation Neuron
Title Neuron
Publication Year 1988-
ISBN/ISSN 0896-6273
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