PubMed · 16437837
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L Holford-Strevens. 1993. The harmonious pulse.. https://doi.org/10.1017/s0009838800040015
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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.
Circadian rhythms in physiology and behavior are regulated by the SCN. When assessed by expression of clock genes, at least 2 distinct functional cell types are discernible within the SCN: nonrhythmic, light-inducible, retinorecipient cells and rhythmic autonomous oscillator cells that are not directly retinorecipient. To predict the responses of the circadian system, the authors have proposed a model based on these biological properties. In this model, output of rhythmic oscillator cells regulates the activity of the gate cells. The gate cells provide a daily organizing signal that maintains phase coherence among the oscillator cells. In the absence of external stimuli, this arrangement yields a multicomponent system capable of producing a self-sustained consensus rhythm. This follow-up study considers how the system responds when the gate cells are activated by an external stimulus, simulating a response to an entraining (or phase-setting) signal. In this model, the authors find that the system can be entrained to periods within the circadian range, that the free-running system can be phase shifted by timed activation of the gate, and that the phase response curve for activation is similar to that observed when animals are exposed to a light pulse. Finally, exogenous triggering of the gate over a number of days can organize an arrhythmic system, simulating the light-dependent reappearance of rhythmicity in a population of disorganized, independent oscillators. The model demonstrates that a single mechanism (i.e., the output of gate cells) can account for not only free-running and entrained rhythmicity but also other circadian phenomena, including limits of entrainment, a PRC with both delay and advance zones, and the light-dependent reappearance of rhythmicity in an arrhythmic animal.
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