Modulation of glycinergic synaptic current kinetics by octanol in mouse hypoglossal motoneurons

Octanol-induced changes in the kinetics of glycinergic inhibitory postsynap tic currents (IPSCs) were investigated by whole-cell recording from hypoglo ssal motoneurons in mouse brainstem slices. Octanol (1 mM) prolonged the de cay time constants (tau(decay)) of stimulus-evoked IPSCs (e-IPSCs) by 202+/ -67% (SE). The depression of e-IPSC amplitudes was dose-dependent with an E C50 of 475 mu M. Octanol also reduced the amplitude and prolonged the decay time constant of glycinergic currents evoked by local pressure ejection of glycine (I-gly). Replacement of extracellular Na+ by choline and applicati on of the specific glycine transporter GLYT1 inhibitor, sarcosine, lengthen ed tau(decay) of I-gly, but did not change the decay time constants of e-IP SCs. Intracellular acidification by the weak organic acid salt sodium propi onate (30 mM) reduced the e-IPSC amplitude by 22+/-9% and prolonged tau by 18+/-6%. Sodium propionate also prolonged the decay time constants of I-gly by 28+/-11%. The observed effects on decay kinetics were much smaller than those caused by octanol. The data show that octanol prolongs the decay tim e course of glycinergic synaptic currents by mechanisms independent of glyc ine uptake or intracellular acidification. We conclude that the effects wer e most probably due to direct action on postsynaptic glycine receptors.