L-type calcium channels but not N-methyl-D-aspartate receptor channels mediate rhythmic activity induced by cholinergic agonist in motoneurons from turtle spinal cord slices.

Rhythmic activity induced by different combinations of N-methyl-D-aspartate (NMDA), serotonin (5-HT), muscarine and D-tubocurarine was monitored intracellularly in lumbar motoneurons in a slice preparation from adult turtles. Low concentration of NMDA (7.5-15 microM) combined with 5-HT (10-80 microM) induced rhythmic motoneuron discharge which was underlied by intrinsic voltage oscillations resistant to tetrodotoxin. This oscillatory activity was abolished by 2-amino-5-phosphonopentanoic acid (AP5), a competitive blocker of NMDA receptors and by nifedipine a selective blocker of L-type calcium channels. In contrast, rhythmicity induced by the cholinergic agents muscarine and d-tubocurarine was abolished by nifedipine but not by AP5 nor by high [Mg2+]o. These results show that different receptor agonists induce intrinsic oscillations in mature motoneurons by independent routes. Each oscillatory mechanism depends on L-type calcium channels but only NMDA/5-HT-induced oscillations depend on voltage-sensitive NMDA-activated ionophores.