The effect of antivitamin B6 administration on gamma-aminobutyric acid metabolism in retina and electroretinogram.
The effect of several antivitamin B6 on gamma-aminobutyric acid (GABA) metabolism was studied in the rat retina. The rat electroretinogram (ERG) was also recorded after administration of these drugs. Aminooxyacetic acid (AOAA) and hydrazine administration increased the GABA content and inhibited the GABA degrading enzyme, GABA transaminase in retina. In addition, there drugs elongated the peak latency of the oscillatory potential in the rat ERG. In contrast, 4-deoxypyridoxine (DOP) or isonicotinic acid hydrazide (INAH) administration decreased the GABA content and inhibited the GABA synthesizing enzyme, glutamic acid decarboxylase in retina, and administration of these drugs together with AOAA lessened the degrees of elevation of GABA content and of the elongation of the peak latency produced as compared with AOAA alone, though neither of the former drugs had a significant effect on ERG. The retinal GABA seems to play an important role in relation to the oscillatory potential of ERG.
D000612:4-Aminobutyrate Transaminase / Q000037:antagonists & inhibitors; D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000818:Animals; D004596:Electroretinography; D005968:Glutamate Decarboxylase / Q000037:antagonists & inhibitors; D006834:Hydrazines / Q000494:pharmacology; D007538:Isoniazid / Q000494:pharmacology; D008297:Male; D011736:Pyridoxine / Q000037:antagonists & inhibitors*; D051381:Rats; D012160:Retina / Q000201:enzymology / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D006834:Hydrazines; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D000612:4-Aminobutyrate Transaminase; D005968:Glutamate Decarboxylase; D011736:Pyridoxine; D007538:Isoniazid