29 results match your criteria: "8600 University Boulevard[Affiliation]"
Neurochem Int
October 2012
Laboratory of Neurochemistry, Indiana University School of Medicine, 8600 University Boulevard, Evansville, IN 47712, U.S.A.
GABA receptor binding to mammalian neuronal membranes has been classified into at least 2 subtypes-GABA(A) and GABA(B) binding sites. In catfish brain GABA(A) receptor sites have previously been demonstrated. Evidence is now presented that under appropriate conditions which rule out GABA(A) receptor binding, [(3)H]GABA binds to membranes prepared from catfish brain.
View Article and Find Full Text PDFNeurochem Int
October 2012
Laboratory of Neurochemistry, Indiana University School of Medicine, 8600 University Boulevard, Evansville, IN 47712, U.S.A.
The regulation of glutamic decarboxylase (GAD) activity is undoubtedly the key to the control of the steady-state concentrations of 4-aminobutyric acid (GABA) in the central nervous system. Those factors that might influence GAD activity are reviewed. They include repression and induction of GAD synthesis; the interconversion of the holo- and apo-form of GAD; the availability of substrate and cofactor; the competitive inhibition of GAD by endogenous substances, including GABA; and the involvement of calcium ions in whole-cell preparations.
View Article and Find Full Text PDFSynaptosomal GABA uptake, sodium-dependent GABA binding to synaptic membranes and GABA receptor binding were measured in the cerebral cortex of five inbred strains of mice. These were the SWR/J, BALB/cJ, DBA/1J, C57BL/10J and C3HeB/FeJ strains. A highly significant negative correlation was found to exist between GABA uptake and blood pressure (r = ?0.
View Article and Find Full Text PDFNeurochem Int
October 2012
Laboratory of Neurochemistry, Indiana University School of Medicine, 8600 University Boulevard, Evansville, IN 47712, U.S.A.
With a view to finding potential GABA-mimetics, the effects of a number of structural analogues of GABA were studied on three parameters associated with GABA neural transmission of rat brain. These were (1) the binding of [(3)H]GABA to its receptor, (2) the binding of [(3)H]GABA to its transporter (sodium-dependent binding), and (3) the activity of GABA aminotransferase. Thirteen of the 21 compounds tested competitively inhibited both the low and the high affinity GABA receptor binding components.
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