Intracellular calcium increase induced by GABA in visual cortex of fetal and neonatal rats and its disappearance with development.
To address the question of whether gamma-aminobutyric acid (GABA) induces a change in the concentration of Ca2+ in neurons of the developing visual cortex, and if so, to elucidate a developmental profile of such a GABA-induced change, we measured intracellular Ca2+ signals using microscopic fluorometry in visual cortical slices loaded with rhod-2. The slices were prepared from rat fetuses of embryonic day 18 (E18) and rat pups of postnatal days 0-30 (P0-P30). Application of GABA through the perfusate at 100 microM induced a marked rise in intracellular Ca2+ signals in the cortical plate and subplate at E18 and P0-P2. After P5 the GABA-induced rise in Ca2+ dramatically reduced, and at P20 and thereafter it became undetectable. At E18 and P0-P2 an agonist for GABAA receptor, muscimol, induced a Ca2+ rise in the same way as did GABA, while a GABAB receptor agonist, baclofen, did not induce any significant rise in Ca2+ signals. Also, a GABAA receptor antagonist, bicuculline, blocked the GABA-induced rise in Ca2+ signals. These results indicate that the Ca2+ rise is triggered by activation of GABAA receptors. The application of Ni2+ at a concentration high enough to block all types of voltage-dependent CA2+ channels prevented the Ca2+ signals from increasing in response to GABA application, suggesting that Ca2+ may be influxed through such channels following depolarization evoked by GABA.