GABA May Act as a Self-Limiting Trophic Factor at Developing Synapses

Arnold R. Kriegstein, and David F. Owens

A. R. Kriegstein is in the Department of Neurology and Department of Pathology and at the Center for Neurobiology and Behavior, Columbia College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA. E-mail: ark17{at}columbia.edu
D. F. Owens is in the Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, NIH, Building 36, 36 Convent Drive, Bethesda, MD 20892, USA. E-mail: owensd{at}nind.nih.gov

Abstract:

Early in development, synapses with glycine or -aminobutyric acid (GABA)-gated chloride channels exhibit the ability to depolarize postsynaptic cells. As the synapses mature and the gradient of chloride ions across the cell membrane is altered, these neurotransmitters signal an inhibitory response, hyperpolarizing the membrane and decreasing neuronal excitability. Kriegstein and Owens discuss how GABA-stimulated up-regulation of the expression of the potassium chloride cotransporter KCC2 may be the mechanism underlying this synaptic switch.

Citation:
A. R. Kriegstein, D. F. Owens, GABA May Act as a Self-Limiting Trophic Factor at Developing Synapses. Science's STKE (2001), http://stke.sciencemag.org/cgi/content/full/OC_sigtrans;2001/95/pe1.

© 2001 American Association for the Advancement of Science

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