DEVELOPMENT OF GLYCINE-GATED AND GABA-GATED CURRENTS IN RAT SPINAL MOTONEURONS

1. Developmental changes in glycine- acid gamma-aminobutyric acid (GABA)-activated currents were studied in spinal motoneurons of embryonic and neonatal rats with the use of whole cell recording techniques. 2. Pressure ejection of glycine or GABA onto motoneuron somata produced Cl--mediated inward currents and membrane depolarizations. During embryonic development, the average amplitude of GABA-gated currents was threefold larger than that of glycine-gated currents, but as a result of a large eightfold postnatal increase in glycine-activated currents, similar currents were produced by both amino acids after birth. 3. At all ages the decay of glycine- and GABA-gated currents best fit one-exponential curve, and their time constants were similar. The average decay time constant decreased by twofold after birth. 4. The ionic specificity of glycine- and GABA-gated channels was studied to determine whether the large amplitude of GABA-activated currents in embryonic motoneurons resulted from the contribution of an outward HCO3- movement. Manipulations of Cl- and HCO3- concentrations produced changes in the reversal potentials of glycine and GABA that were similar to the calculated changes in the equilibrium potentials of Cl-. This suggested that glycine- and GABA-gated currents were Cl- specific, and HCO3- movement did not contribute more to the current generated by GABA than that produced by glycine. 5. Glycine- and GABA-gated currents were associated with severalfold increases in membrane conductance. The conductance increase generated by GABA in embryonic motoneurons was sevenfold larger than that generated by glycine, but similar conductance changes were produced by both amino acids after birth. 6. Despite the induced depolarizations, activation of glycine and GABA receptors was associated with inhibition of spontaneous potentials and decreased motoneuron excitability. Our data aug gested that glycine and GABA acted as inhibitory neurotransmitters by increasing Cl- conductance and effectively shunting incoming excitatory currents.