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A Volume in the THE HISTORY OF NEUROSCIENCE IN AUTOBIOGRAPHY by Larry R. Squire (Eds.)

By Larry R. Squire (Eds.)

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JNeurosciRes 1989;23:129-135. Aprison MH, Lipkowitz KB. Molecular modeling of the weak glycine antagonist iso-Thao. J Neurosci Res 1991;30:442-446. Aprison MH, Lipkowitz KB. Muscimol and AT^AT-dimethylmuscimol: From a GABA agonist to a glycine antagonist. J Neurosci Res 1992;31:166-174. Aprison MH, Werman R. A combined neurochemical and neurophysiological approach to the identification of CNS transmitters. In Ehrenpreis S, Solnitzky OC, eds. Neuroscience research. New York: Academic Press, 1968; 2:143-174.

D: An electrostatic attraction between LYS200 and the lone pair electrons on 0 1 7 . E: A bidentate electrostatic attraction of ARG271 with the negative carbonyl oxygen. F: A charge-transfer complex between TYR202 and the aromatic moiety on strychnine. I l l - Representation of zwitterionic GABA binding to its receptor site. Key electrostatic and hydrogen bonding interactions are labeled A - F as in I & II. IV - Representation of R5135 binding in the GABA receptor site. Stabihzing interactions from electrostatic and hydrogen bonding are labeled as sites A-C.

The fact that the assay was not dependent on the presence of extracellular sodium was strong support that glycine was not binding to a transporter. An additional important observation that came from these studies was the result that although the cerebral cortex had the highest B^^^ value, it was known to have very few inhibitory glycinergic synapses. The significance of these data would not be recognized for nearly a decade. However, we suggested that glycine was binding to sites other than the glycine receptor, and that these other glycine binding sites were sensitive to D-serine.

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