Eur J Neurosci 1989 Jan 01;16:561-571.

Roles of Glycinergic Inhibition and N-Methyl-D-Aspartate Receptor Mediated Excitation in the Locomotor Rhythmicity of One Half of the Xenopus Embryo Central Nervous System.

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Recent investigations into the neural basis for swimming in Xenopus embryos have pointed to central roles played by N-methyl-D-aspartate (NMDA) receptor-mediated excitation acting within and glycinergic reciprocal inhibition acting between motor systems for the muscular antagonists on the two sides of the CNS. A 'reduced' preparation consisting of only one half of the CNS divided sagittally along its midline is used here to examine the basis for rhythmicity within each side in the absence of reciprocal connections. Divided preparations transected rostrally at levels between the otic capsule and the obex can all generate a rhythmic pattern of motor discharge similar to that which underlies swimming. All rhythm generation is blocked by the NMDA antagonist (+/-)-2-amino-5-phosphonovaleric acid (AP5) at 20 microM. However, neither glycinergic nor GABAergic inhibition is required for a basic rhythmicity since some rhythm persists in the presence of 10 microM strychnine and 50 microM bicuculline, though it is no longer sustained. In the divided spinal cord alone, rhythm generation requires extracellular Mg2+. If the most caudal segment of the divided hindbrain is left attached, extracellular Mg2+ is required only if strychnine is present. If more of the hindbrain is included, extracellular Mg2+ is no longer necessary for rhythm generation even in the presence of strychnine. It seems that rhythm generation by a single side of the spinal cord requires NMDA receptor-mediated excitation together with the voltage dependency conferred on it by extracellular Mg2+, but not inhibition in order to occur. As more of the hindbrain is left attached, the requirement for extracellular Mg2+ becomes progressively less strong. For sustained rhythm generation, one side of the CNS requires both excitation and glycinergic inhibition.

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