Premium
Inhibition of Brain Glutamate Decarboxylase Activity Is Related to Febrile Seizures in Rat Pups
Author(s) -
Arias Clorinda,
Valero Hilda,
Tapia Ricardo
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb09320.x
Subject(s) - glutamate decarboxylase , glutamate receptor , carboxy lyases , neuroscience , pharmacology , medicine , chemistry , psychology , biochemistry , enzyme , receptor
Because previous work showed that in the newborn brain, but not in the adult brain, glutamate decarboxylase (GAD) is notably susceptible to heat, we have studied the possible involvement of GAD inhibition in febrile convulsions and the related changes in γ‐aminobutyric acid (GABA) content. Rats of different ages were subjected to hyperthermia, and GAD activity was determined in brain homogenates by measuring the release of 14 CO 2 from labeled glutamate and by measuring the formation of GABA. The latter method gave considerably lower values than the former in the youngest rats, and was considered more reliable. With this method, we found a 37–48% inhibition of GAD activity in rat pups 2–5 days old, which showed febrile seizures at progressively higher body temperatures, whereas in 10‐ and 15‐day‐old animals, which did not show convulsions, GAD activity was not affected by hyperthermia. Whole‐brain GABA levels, however, did not change at any age. In contrast to GAD, choline acetyltransferase and lactic dehydrogenase activities were not altered by hyperthermia at any of the ages studied. These results suggest that a decreased efficiency of the inhibitory neurotransmission mediated by GABA, consequent to the inhibition of GAD activity, may be a factor related to febrile convulsions.