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 motoneuron al output during such behaviours as locomotion. A conductance through L-typ e calcium channels has been implicated as an essential component in the tra nsduction of motoneuronal input to output during locomotion. Given the deve lopmental changes in calcium currents occurring postnatally in some neurons , and the increasing interest in the study of spinal locomotor output in ne onatal preparations, experiments were conducted to investigate the postnata l developmental of L-type calcium channels in mouse motoneurons. This was a ssessed both physiologically, using a chemically induced rhythmic motor out put, and anatomically, using immunohistochemical methods. The electrophysio logical 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 ha d no effect on this ventral root bursting in postnatal day (P) P2-P5 animal s, but reversibly reduced the amplitude and/or burst duration of this activ ity in animals greater than P7. The immunohistochemical evidence demonstrat ed a dramatic change in the cellular profile of both the alpha(1C) and alph a(1D) subunits of L-type calcium channels during postnatal development; the labelling of both subunits increased with age, approximating the adult pat tern by P18. These results demonstrate that in the spinal cord, the L-type calcium channel profile develops both physiologically and anatomically in t he early postnatal period. This development parallels the development of th e mature functional behaviours of weight bearing and walking, and may be ne cessary for the production of complex motor behaviour in the mature mammal.