Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. Signal., 24 November 2009
Vol. 2, Issue 98, p. ec380
[DOI: 10.1126/scisignal.298ec380]

EDITORS' CHOICE

Neuroscience Dysbindin Function in Synaptic Homeostasis

Stella M. Hurtley

Science, AAAS, Cambridge CB2 1LQ, UK

Homeostatic signaling systems are widely believed to stabilize neural function over prolonged periods of time. However, the molecular mechanisms of homeostatic signaling in the nervous system are largely unknown, and direct links between defective homeostatic signaling and disease-causing genes remain obscure. Dickman and Davis performed a large-scale, electrophysiology-based genetic screen for mutations that specifically disrupt synaptic homeostasis. DTNBP1 is one of two genes that are most strongly and consistently associated with schizophrenia susceptibility in humans. The Drosophila homolog of DTNBP1 (dysbindin) was identified in the screen and was found to function during synapse development, baseline neurotransmission, and synaptic homeostasis. Dysbindin altered the calcium dependence of vesicle release and was essential in the presynaptic neuron for both the induction and expression of synaptic homeostasis.

D. K. Dickman, G. W. Davis, The schizophrenia susceptibility gene dysbindin controls synaptic homeostasis. Science 326, 1127–1130 (2009). [Abstract] [Full Text]

Citation: S. M. Hurtley, Dysbindin Function in Synaptic Homeostasis. Sci. Signal. 2, ec380 (2009).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882