Xenopus embryos immobilized in tubocurarine respond to natural skin stimulation with fictive swimming. This can also occur in saline without Mg2+ and is blocked by NMDA antagonists. Ventral spinal cord neurons which are rhythmically active during swimming are depolarized by bath applied N-methyl-D-aspartate (NMDA) (in 1 μM tetrodotoxin (TTX) to block indirect effects). By using current clamp techniques this depolarization is shown to be partially blocked by 0.5 and 1 mM Mg2+ in a voltage-dependent manner similar to that described in cultured neurons.
Mg2+ partially and reversibly reduces the slow NMDA-mediated component of excitatory post-synaptic potentials (EPSPs) in ventral neurons. However, in 1 mM Mg2+ fictive swimming can still be evoked by natural stimulation. The frequency of swimming is slightly lower than in nominally 0 mM Mg2+, but the pattern of ventral root activity and synaptic drive to ventral neurons seems little affected. Fictive swimming can also be induced by applying NMDA to spinal preparations. In 0 mM Mg2+, such rhythmic activity is unstable and transient over a narrow NMDA concentration range. In 0.5 mM Mg2+, continuous rhythmic activity is induced over a wide range of NMDA concentrations. Lower spinal preparations need higher NMDA concentrations to induce activity.
We conclude that the neurons rhythmically active in swimming have NMDA receptor channels which show a voltage dependent block in the presence of Mg2+. However, while Mg2+ exerts a powerful stabilizing influence on rhythmic activity induced in spinal embryos by exogenous NMDA, its influence on ‘naturally’ evoked fictive swimming is less clear. The fictive swimming machinery in the brain and spinal cord can produce stable swimming with or without Mg2+ induced voltage dependency of the NMDA channels.