Development of L-type calcium channels and a nifedipine-sensitive motor activity in the postnatal mouse spinal cord.

Intrinsic membrane properties are important in the regulation of motoneuronal output during such behaviours as locomotion. A conductance through L-type calcium channels has been implicated as an essential component in the transduction of motoneuronal input to output during locomotion. Given the developmental changes in calcium currents occurring postnatally in some neurons, and the increasing interest in the study of spinal locomotor output in neonatal preparations, experiments were conducted to investigate the postnatal development of L-type calcium channels in mouse motoneurons. This was assessed both physiologically, using a chemically induced rhythmic motor output, and anatomically, using immunohistochemical methods. The electrophysiological data were obtained during rhythmic bursting produced by application of N-methyl-D-aspartate (NMDA) and strychnine to the isolated spinal cord at various postnatal ages. The L-type calcium channel blocker nifedipine has no effect on this ventral root bursting in postnatal day (P) P2-P5 animals, but reversibly reduced the amplitude and/or burst duration of this activity in animals greater than P7. The immunohistochemical evidence demonstrates a dramatic change in the cellular profile of both the alpha1C and alpha1D subunits of L-type calcium channels during postnatal development; the labelling of both subunits increases with age, approximating the adult pattern by P18. These results demonstrate that in the spinal cord, the L-type calcium channel profile develops both physiologically and anatomically in the early postnatal period. This development parallels the development of the mature functional behaviours of weight bearing and walking, and may be necessary for the production of complex motor behaviour in the mature mammal.