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In addition to causing a slow depolarization, thyrotropin-releasing hormone (TRH, 5–10 μM) evoked synaptic activity in antidromically identified motoneurons in thin transverse neonatal rat spinal cord slices. The synaptic activity but not the slow depolarization was reversibly abolished by TTX or low Ca 2+ /high Mg 2+ solution. Furthermore, the TRH-induced synaptic activity was eliminated by the glutamate receptor antagonist kynurenic acid (0.5 or 1 mM) and/or the glycine receptor antagonist strychnine (1 μM). Our results indicate that in addition to depolarizing motoneurons, TRH modifies the activity of spinal interneurons which may secondarily alter the activity of motoneurons.

When superfused onto rat hippocampal slices, glycine (0.1-0.5 mM) potentiated the depolarization induced by pressure application of NMDA in normal Krebs solution and the synaptic discharge evoked by stimulation of the Schaffer collateral-commissural inputs to the CA1 pyramidal neurons bathed in Mg2+-free media; the effects were not prevented by strychnine. In addition, glycine partially reversed the blocking effect of D-2-amino-5-phosphonovalerate (AP5) on N-methyl-D-aspartate (NMDA)-induced depolarization. These results show that glycine at relatively high concentrations potentiates the NMDA-mediated response in hippocampal slices.