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The metabolism of radioactive glutamic acid in normal and epileptic cat brain

University of British Columbia

The indirect in vivo inhibition of the enzyme glutamic acid decarboxylase (GAD) by either vitamin B-6 deficiency or the administration of vitamin B-6 antimetabolites decreases the conversion of glutamic acid to gamma aminobutyric acid (GABA) in brain. This decrease is a concomitant to the occurrence of seizures resembling grand mal. The in vivo reactivation of GAD by vitamin B-6 administration and/or by the topical application of GABA to the brain surface reduces the intensity of the convulsions. Because of this, it has been suggested that a decrease in the conversion of glutamic acid to GABA in brain may be a factor in the precipitation and maintenance of epileptic seizures. In order to investigate this suggestion, the in vivo metabolism of C-14 labelled glutamic acid to GABA and other amino acids was quantitatively determined in various brain areas of several normal cats; a cat with a epileptogenic lesion in the left motor cortex produced by alumina cream; and one cat in status epilepticus. Throughout most non-epileptogenic brain areas there were similar rates of conversion of glutamic acid to GABA, aspartic acid and glutamine. Notable exceptions to this consistency were found repeatedly in the quadri-geminal plate, thalamus and putamen-globus pallidus where there was a higher conversion of glutamic acid to GABA. No apparent consistency in the degree of conversion of glutamic acid to the other amino acids could be discerned throughout the brain of the cat in status epilepticus. In the epileptogenic lesion there was a decrease in the conversion of glutamic acid to GABA, which is compatible with the suggestion that a reduction in GABA levels increases the degree of brain excitability.

Text

2011-11-23

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http://hdl.handle.net/2429/39233

Neuroscience

University of British Columbia

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