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Bath application of N-methyl-D-aspartate (NMDA), kainate or quisqualate to Xenopus embryos depolarized spinal cord motoneurones and reduced their input resistance in both normal salines and salines containing 20 mM-Mn2+ and 0.5 mM-Ca2+, or 2 X 10(-6) M-tetrodotoxin. This suggests that motoneurones possess all three types of excitatory amino acid receptor. These receptors have similar specificities to excitatory amino acid antagonists as those occurring in adult frog and cat spinal cords. Application of 30-40 microM-NMDA or 5-6.5 microM-kainate to the medium bathing spinalized embryos can cause a sustained patterned motor output similar to that of swimming evoked by natural stimulation of intact animals. At these concentrations NMDA and kainate depolarized motoneurones by 19.0 +/- 1.80 (mean +/- S.E. of mean) and 18.0 +/- 2.00 mV respectively and decreased their input resistance by 23.0 +/- 2.82% and 24.0 +/- 3.46%. These changes are similar to those associated with the tonic excitation which motoneurones receive during naturally evoked swimming. Bath application of 5-8 microM-quisqualate to spinal embryos can also cause a sustained motor output. However, this was different to that evoked by NMDA and kainate and was inappropriate for swimming. When applied to intact animals during swimming both 2-3 mM-cis-2,3-piperidine dicarboxylic acid (PDA) and 0.5 mM-gamma-D-glutamylglycine (DGG) selectively blocked the tonic excitation of motoneurones and in doing so abolished the motor output of the spinal cord. 50-200 microM-2-amino-5-phosphonovaleric acid reduced the tonic excitation but to a lesser extent than either PDA or DGG. The tonic excitation of motoneurones which occurs during swimming therefore appears to be mediated via an endogenous excitatory amino acid transmitter which acts on NMDA and kainate receptors.

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