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) indu ces a change in the concentration of Ca2+ in neurons of the developing visual cortex, and if so, to elucidate a developmental profile of suc h 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) an d rat pups of postnatal days 0-30 (P0-P30). Application of GABA throug h the perfusate at 100 mu M induced a marked rise in intracellular Ca2 + signals in the cortical plate and subplate at E18 and P0-P2. After P 5 the GABA-induced rise in Ca2+ dramatically reduced, and at P20 and t hereafter it became undetectable. At E18 and P0-P2 an agonist for GABA , receptor, muscimol, induced a Ca2+ rise in the same way as did GABA, while a GABA(B) receptor agonist, baclofen, did not induce any signif icant rise in Ca2+ signals. Also, a GABA(A) receptor antagonist, bicuc ulline, blocked the GABA-induced rise in Ca2+ signals. These results i ndicate that the Ca2+ rise is triggered by activation of GABA(A) recep tors. The application of Ni2+ at a concentration high enough to block all types of voltage-dependent Ca2+ channels prevented the Ca2+ signal s from increasing in response to GABA application, suggesting that Ca2 + may be influxed through such channels following depolarization evoke d by GABA.