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Molecular and Cellular Biology, August 2006, p. 5728-5734, Vol. 26, No. 15
0270-7306/06/$08.00+0 doi:10.1128/MCB.00237-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of Genetics and Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115,1 Department of Neurology, Mount Sinai School of Medicine, New York, New York 10029,2 Department of Neurology and Program in Developmental and Stem Cell Biology, University of California, San Francisco, California 941433
Received 8 February 2006/ Returned for modification 7 April 2006/ Accepted 22 May 2006
Glycine receptors are ligand-gated chloride channels that mediate inhibitory neurotransmission in the adult nervous system. During development, glycine receptor alpha 2 (GlyR
2) is expressed in the retina, in the spinal cord, and throughout the brain. Within the cortex, GlyR
2 is expressed in immature cells and these receptors have been shown to be active and excitatory. In the developing retina, inhibition of glycine receptor activity prevents proper rod photoreceptor development. These data suggest that GlyR
2, the developmentally expressed glycine receptor, may play an important role in neuronal development. We have generated mice with a targeted deletion of glycine receptor alpha 2 (Glra2). Although these mice lack expression of GlyR
2, no gross morphological or molecular alterations were observed in the nervous system. In addition, the cerebral cortex does not appear to require glycine receptor activity for proper development, as Glra2 knockout mice did not show any electrophysiological responses to glycine.
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