XXXX dual modulatory actions on spontaneous postsynaptic currents in spinal motoneurons.

@entity1024 @entity2227 @entity1246 @entity2228 @entity167 @entity143 @entity35 @entity1068
Recently we have shown that acute @entity1068 ( @entity167 ) exposure suppresses dorsal root-evoked synaptic potentials in spinal motoneurons. To examine the synaptic mechanisms underlying the reduced excitatory activity, @entity167 actions on properties of action potential-independent miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) were studied in spinal motoneurons of newborn @entity35 . Properties of mEPSCs generated by activation of @entity1024 receptors (NMDARs) and non- @entity143 receptors and of mIPSCs mediated by @entity2228 and @entity1246 -A receptors (GlyR and @entity1246 (A)R) were examined during acute exposure to 70 and 200 mM @entity167 . In the presence of 70 mM @entity167 , the frequency of NMDAR- and non-NMDAR-mediated mEPSCs decreased to 53 +/- 5 and 45 +/- 7% (means +/- SE) of control values, respectively. In contrast, the frequency of GlyR- and @entity1246 (A)R-mediated mIPSCs increased to 138 +/- 15 and 167 +/- 23% of control, respectively. Based on the quantal theory of transmitter release, changes in the frequency of miniature currents are correlated with changes in transmitter release, suggesting that @entity167 decreased presynaptic @entity2227 release and increased the release of both @entity2228 and @entity1246 . @entity167 did not change the amplitude or rise and decay times of either mEPSCs or mIPSCs, indicating that the presynaptic changes were not associated with changes in the properties of postsynaptic receptors/channels. Acute exposure to 200 mM @entity167 increased mIPSC frequency two- to threefold, significantly higher than the increase induced by 70 mM @entity167 . However, the decrease in mEPSC frequency was similar to that observed in 70 mM @entity167 . Those findings implied that the regulatory effect of @entity167 on @entity2228 and @entity1246 release was dose-dependent. Exposure to the higher @entity167 concentration had opposite actions on mEPSC and mIPSC amplitudes: it attenuated the amplitude of NMDAR- and non-NMDAR-mediated mEPSCs to ~80% of control and increased GlyR- and @entity1246 (A)R-mediated mIPSC amplitude by ~20%. @entity167 -induced changes in the amplitude of postsynaptic currents were not associated with changes in their basic kinetic properties. Our data suggested that in spinal networks of newborn @entity35 , @entity167 was more effective in modulating the release of excitatory and inhibitory neurotransmitters than changing the properties of their receptors/channels.
