scholarly journals A new microassay method for L-glutamic acid decarboxylase (GAD) activity

1974 ◽  
Vol 24 ◽  
pp. 79
Author(s):  
Hiroshi Kimura ◽  
Klnya Kuriyama
1974 ◽  
Vol 52 (5) ◽  
pp. 952-959 ◽  
Author(s):  
N. M. van Gelder

Determinations of glutamate dehydrogenase (GDH), glutamic acid decarboxylase (GAD), and GABA aminotransferase (GABA-T) in the epileptogenic (cobalt) mouse cortex revealed a fall in the activities of GDH and GABA-T and an increase in GAD. However, of the three enzymes, only changes in GDH appeared to coincide with the entire period that animals were epileptic. The decrease in GABA-T was observed in the first week following the onset of cobalt-induced epilepsy but the activity of this enzyme had returned to normal before all epileptic signs had disappeared. On the other hand, the rise in GAD activity was observed 3–4 days after epilepsy had become established. Injections of taurine to animals did not influence the above findings but might have slowed recovery to normal enzyme values.


1976 ◽  
Vol 54 (2) ◽  
pp. 79-82 ◽  
Author(s):  
G. Tunnicliff ◽  
R. F. Butterworth ◽  
Y. Tsukada ◽  
A. Barbeau

Recent reports of the in vivo action of L-dihydroxyphenylalanine (L-DOPA) on glutamic acid decarboxylase (GAD) activity are contradictory. This investigation was undertaken to clarify the situation. Both acute (100 mg/kg and 1 g/kg) and chronic (1 g/kg) administration of L-DOPA to rats failed to produce any alteration in the activity of striatal or retinal GAD activity. These results are discussed in the light of a report relating L-DOPA therapy to modification of GAD activity in Parkinson's disease.


2012 ◽  
Vol 225 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Alan L. Pehrson ◽  
Corina O. Bondi ◽  
Nelson K. B. Totah ◽  
Bita Moghaddam

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