[Role of Ca(2+) in the pacemaker-like property of spinal motoneurons]

It is generally accepted that locomotion in vertebrate species is produced by signals coded and integrated by neurons of the spinal cord. In fact, the basic features of locomotion, including patterns and rhythms, are generated by a network of neurons called the CPG (central pattern generator) essentially localized in the lumbar segments of the spinal cord. However, the detailed mechanisms underlying the rhythmic aspect of CPG-generated locomotion are not fully understood. Here, we report data of studies that focus on the role of Ca(2+)-related mechanisms involved in the expression of the pacemaker property of lumbar motoneurons that innervate the hindlimbs. In fact, it has become increasingly clear that Ca(2+) plays a determinant function in the expression of this active and conditional rhythmic property. In addition to NMDA-mediated currents (NMDA is an agonist of the calcium permeable ionotropic glutamatergic receptor) and to a Ca(2+)-dependent K(+) current that were found twenty years ago to contribute to intrinsic voltage oscillations in motoneurons, a pivotal role for voltage-gated channels (e.g., CaV1.3) and intracellular Ca(2+) concentrations ([Ca(2+)]i) have recently been shown. Increasing evidence of a role for metabotropic receptor subtypes, calmodulin (a calcium binding protein), ryanodine and IP3-sensitive intracellular stores of Ca(2+) suggests that additional mechanisms are yet to be identified. A detailed understanding of the complex role of Ca(2+) in mediating the auto-rhythmic property of spinal neurons may contribute to the development of novel therapeutic approaches to induce locomotion after spinal cord injury.