Involvement of calcium in rhythmic activity induced by disinhibition in cultured spinal cord networks

Disinhibition of rat spinal networks induces a spontaneous rhythmic bursting activity. The major mechanisms involved in the generation of such a bursting are intrinsic neuronal firing of a subpopulation of interneurons, recruitment of the network by recurrent excitation, and autoregulation of neuronal excitability. We have combined whole cell recording with calcium imaging and flash photolysis of caged-calcium to investigate the contribution of [Ca(2+)](i) to rhythmogenesis. We found that calcium mainly enters the neurons through voltage-activated calcium channels and N-methyl-D-aspartate (NMDA) channels as a consequence of the depolarization during the bursts. However, [Ca(2+)](i) could neither predict the start nor the termination of bursts and is therefore not critically involved in rhythmogenesis. Also calcium-induced calcium release is not involved as a primary mechanism in bursting activity. From these findings, we conclude that in the rhythmic activity induced by disinhibition of spinal cord networks, the loading of the cells with calcium is a consequence of bursting and does not functionally contribute to rhythm generation.