-transparent.png){kind=logo}
The inactivation of gamma-aminobutyrate (GABA)-transaminase by the highly specific and potent neurotoxin gabaculine leads to different neurochemical consequences in the chick brain as opposed to the chick retina. In the brain, GABA levels continually climb, reaching approximately eightfold increases over control values after 24 h. The elevation in GABA levels leads to a time-dependent and coincident fall in glutamate decarboxylase and cysteine-sulfinate decarboxylase activities, to approximately 50% of control values. On the other hand, in the retina GABA levels only increase to a plateau level two- to threefold that of control after inactivation of GABA-transaminase. Furthermore, although the glutamate decarboxylase activity decreases to about 50% of control values, cysteinesulfinate decarboxylase activity is not affected. These studies show that the processing of GABA in the retina differs from that in the brain, and that cysteinesulfinate and glutamate decarboxylase activity probably reside in different enzyme molecules in the retina, although they may reside in the same enzyme in the brain.
R R Rando, and
J Coburn, and
D Parkinson
September 1987,
Brain research,
R R Rando, and
J Coburn, and
D Parkinson
January 1988,
Synapse (New York, N.Y.),
R R Rando, and
J Coburn, and
D Parkinson
October 1979,
Neuropharmacology,
R R Rando, and
J Coburn, and
D Parkinson
August 1998,
The European journal of neuroscience,
R R Rando, and
J Coburn, and
D Parkinson
July 2006,
Bioorganic & medicinal chemistry letters,
R R Rando, and
J Coburn, and
D Parkinson
January 1984,
Progress in clinical and biological research,
R R Rando, and
J Coburn, and
D Parkinson
January 1979,
Advances in experimental medicine and biology,
R R Rando, and
J Coburn, and
D Parkinson
February 1998,
Molecular neurobiology,
R R Rando, and
J Coburn, and
D Parkinson
June 1992,
Biochemical pharmacology,
R R Rando, and
J Coburn, and
D Parkinson
September 1993,
Neurochemical research,
