Glutamic acid decarboxylase (GAD)67, but not GAD65, is constitutively expressed during development and transiently overexpressed by activity in the granule cells of the rat.

摘要

gamma-Aminobutyric acid (GABA)-mediated neurotransmission from the granule cells to CA3 is transiently expressed during the first 3 weeks of age in the rat. In the adult, seizures provoke this inhibitory signaling to reappear. To gain insight into the origin of GABA in these cells, we explored the expression of both isoforms of glutamic acid decarboxylase (GAD, 65 and 67 kDa), during development and after seizures in the adult rat. We found that GAD(67), but not GAD(65), is expressed in the mossy fibers of developing rats. In adults, GAD(67) is no longer detectable, unless seizures are induced. By contrast, GAD(65) is neither expressed in granule cells nor in their mossy fibers at any age nor after seizures, despite the presence of GAD(65) mRNA, confirmed by reverse transcription-polymerase chain reaction in situ.