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

1. Developmental changes in glycine- acid gamma-aminobutyric acid (GAB A)-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 C l--mediated inward currents and membrane depolarizations. During embry onic development, the average amplitude of GABA-gated currents was thr eefold larger than that of glycine-gated currents, but as a result of a large eightfold postnatal increase in glycine-activated currents, si milar currents were produced by both amino acids after birth. 3. At al l ages the decay of glycine- and GABA-gated currents best fit one-expo nential curve, and their time constants were similar. The average deca y time constant decreased by twofold after birth. 4. The ionic specifi city of glycine- and GABA-gated channels was studied to determine whet her the large amplitude of GABA-activated currents in embryonic motone urons resulted from the contribution of an outward HCO3- movement. Man ipulations of Cl- and HCO3- concentrations produced changes in the rev ersal potentials of glycine and GABA that were similar to the calculat ed changes in the equilibrium potentials of Cl-. This suggested that g lycine- and GABA-gated currents were Cl- specific, and HCO3- movement did not contribute more to the current generated by GABA than that pro duced by glycine. 5. Glycine- and GABA-gated currents were associated with severalfold increases in membrane conductance. The conductance in crease 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 depol arizations, activation of glycine and GABA receptors was associated wi th inhibition of spontaneous potentials and decreased motoneuron excit ability. Our data aug gested that glycine and GABA acted as inhibitory neurotransmitters by increasing Cl- conductance and effectively shunt ing incoming excitatory currents.