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.