Direct and indirect actions of thyrotropin-releasing hormone on neonatal rat motoneurons in vitro

In addition to causing a slow depolarization, thyrotropin-releasing hormone (TRH, 5-10 microM) 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 Ca2+/high Mg2+ 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 microM). Our results indicate that in addition to depolarizing motoneurons, TRH modifies the activity of spinal interneurons which may secondarily alter the activity of motoneurons.