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

Octanol-induced changes in the kinetics of glycinergic inhibitory postsynaptic currents (IPSCs) were investigated by whole-cell recording from hypoglossal motoneurons in mouse brainstem slices. Octanol (1 mM) prolonged the decay 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 EC50 of 475 microM. 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 application of the specific glycine transporter GLYT1 inhibitor, sarcosine, lengthened tau(decay) of I(gly), but did not change the decay time constants of e-IPSCs. Intracellular acidification by the weak organic acid salt sodium propionate (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 time course of glycinergic synaptic currents by mechanisms independent of glycine uptake or intracellular acidification. We conclude that the effects were most probably due to direct action on postsynaptic glycine receptors.