Homeostatic signaling systems are believed to interface with the mechanisms of learning-related plasticity to achieve stable, yet flexible, neural function and animal behavior. The loss or disruption of homeostatic signaling is believed to participate in the cause or progression of many neurological diseases including autism spectrum disorders and epilepsy. Ultimately, clear links between homeostatic signaling and disease will require a detailed molecular understanding of homeostatic signaling systems. Here we identify several novel homeostatic plasticity genes that dramatically extend our understanding of how homeostatic signaling systems stabilize neural function.
Homeostatic signaling systems are believed to interface with the mechanisms of learning-related neural plasticity to achieve stable, yet flexible, neural function and animal behavior. Recently, homeostatic signaling systems are being invoked as contributing to the cause or progression of diverse neurological diseases including Alzheimer's, epilepsy and autisms spectrum disorders. However, the molecular basis for the homeostatic regulation of neural function remains largely unknown. Ultimately, clear links between homeostatic signaling and disease will require a detailed molecular understanding of homeostatic signaling in the nervous system. We have a proven ability to identify new homeostatic signaling genes. Here we propose to characterize three novel, highly conserved homeostatic plasticity genes.
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|Ford, Kevin J; Davis, Graeme W (2014) Archaerhodopsin voltage imaging: synaptic calcium and BK channels stabilize action potential repolarization at the Drosophila neuromuscular junction. J Neurosci 34:14517-25|
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|MÃ¼ller, Martin; Davis, Graeme W (2012) Transsynaptic control of presynaptic CaÂ²âº influx achieves homeostatic potentiation of neurotransmitter release. Curr Biol 22:1102-8|
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