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Ca2+ imaging and (perforated) patch recording were used to analyze the mechanism of GABA- and glycine-induced depolarizations in lumbar motoneurons of spinal cord slices from fetal rats. In fura-2 ester-loaded cells, the agonist-induced depolarizations increased [Ca2+]i by up to 100 nm. The GABA- and glycine-evoked [Ca2+]i transients were suppressed by bicuculline and strychnine, respectively. Their magnitude decreased by ∼50% between embryonic days 15.5 and 19.5. The [Ca2+]i increases were abolished by Ca2+-free superfusate and attenuated by ∼65% by nifedipine, showing that the responses were mediated by voltage-activated Ca2+ channels. The [Ca2+]i rises were potentiated by >300% immediately after removal of Cl− from the superfusate but recovered to values of 50–200% of control during repeated agonist administration in Cl−-free saline. Bumetanide gradually suppressed the [Ca2+]i increases by >75%. Subsequent removal of Cl− reconstituted the responses and increased, upon repeated agonist application, the peak [Ca2+]i rises to values above control. Removal of HCO3− from the Cl−-free (bumetanide-containing) superfusate reversibly abolished both the agonist-induced [Ca2+]i rises and depolarizations that were reestablished by formate anions. In Cl−-containing superfusate, removal of HCO3− decreased both the peak and duration of the agonist-evoked membrane depolarization and [Ca2+]i response. Our findings show that HCO3− efflux has a major contribution to depolarizations mediated by GABAA and glycine receptor-coupled anion channels in prenatal neurons. We hypothesize that the HCO3−-dependent depolarizing component, which is likely to produce an intracellular acidosis, might play an important role during the early postnatal period when the Cl−-dependent component gradually shifts to hyperpolarization.

the journal of neuroscience/the journal of neuroscience

Role of Bicarbonate and Chloride in GABA- and Glycine-Induced Depolarization and [Ca2+]iRise in Fetal Rat MotoneuronsIn Situ