Release of gamma-aminobutyric acid from isolated brain synaptosomes during semicarbazide-induced convulsions.
The in vivo effect of semicarbazide (SC) and aminoxyacetic acid (AOAA) upon gamma-aminobutyric acid (GABA) levels in the synaptosomal fraction, and GABA release from the same fraction were studied in the mouse. The convulsive dose of SC reduced the GABA content in synaptosomes, and when the convulsions were protected by pretreatment with AOAA, the reduced GABA content in synaptosomes rose to or above the normal level. Moreover, the SC treatment decreased the GABA releases from synaptosomes both in a Ca2+-free Ringer's solution and in a high K+ Ringer's solution. When the convulsions were protected by pretreatment with AOAA, the decreased GABA releases in both the conditions rose to or above the normal levels. Therefore, it is suggested that the decrease in GABA release from the nerve endings, because of the decrease of GABA content in the same compartment, is possibly an important factor in the onset of some kinds of convulsions.
D000625:Aminooxyacetic Acid / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology; D008297:Male; D051379:Mice; D011188:Potassium / Q000494:pharmacology; D012640:Seizures / Q000139:chemically induced*; D012663:Semicarbazides / Q000494:pharmacology*; D013574:Synaptosomes / Q000187:drug effects* / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D012663:Semicarbazides; D000625:Aminooxyacetic Acid; D005680:gamma-Aminobutyric Acid; D011188:Potassium; D002118:Calcium