Effects of magnesium on fictive locomotion induced by activation of N-methyl-d-aspartate (NMDA) receptors in the Lamprey spinal cord in vitro

It has previously been demonstrated that an activation of N-methyl-d-aspartate (NMDA) receptors can induce fictive locomotion as well as tetrodotoxin (TTX)-resistant membrane potential oscillations in certain types of neurone in the in vivo preparation of the lamprey spinal cord. These oscillations in individual neurons depend on voltage-sensitive properties of NMDA-activated channels which are only manifested in the presence of Mg²⁺. To evaluate the role of these pacemaker-like oscillations in the generation of locomotion, the motor patterns induced by N-methyl-d,l-aspartate (NMA) before and after removal of Mg²⁺ were compared. It was found that the ventral root burst pattern of fictive locomotion was more irregular after removal of Mg²⁺, particularly at low burst rates. This suggests that the membrane properties underlying the NMDA-induced TTX-resistant membrane potential oscillations are of importance for the generation of a stable and regular locomotor activity in particular at low rates of fictive locomotion. When fictive locomotion was induced instead by an activation of kainate receptors a removal of Mg²⁺ had no effect on the motor pattern. The effects of the two K⁺-channel blockers, tetraethylammonium (TEA) and gallamine were also tested on NMA-induced fictive locomotion. Both compounds caused an increase in the burst frequency. The Mg²⁺-dependent NMDA-induced bistable membrane properties thus appear to be of importance for the operation of the network which generates the locomotor pattern.