Contributions of intrinsic motor neuron properties to the production of rhythmic motor output in the mammalian spinal cord.
Motor neurons are endowed with intrinsic and conditional membrane properties that may shape the final motor output. In the first half of this paper we present data on the contribution of I(h), a hyperpolarization-activated inward cation current, to phase-transition in motor neurons during rhythmic firing. Motor neurons were recorded intracellularly during locomotion induced with a mixture of N-methyl-D-aspartate (NMDA) and serotonin, after pharmacological blockade of I(h). I(h) was then replaced by using dynamic clamp, a computer program that allows artificial conductances to be inserted into real neurons. I(h) was simulated with biophysical parameters determined in voltage clamp experiments. The data showed that electronic replacement of the native I(h) caused a depolarization of the average membrane potential, a phase-advance of the locomotor drive potential, and increased motor neuron spiking. Introducing an artificial leak conductance could mimic all of these effects. The observed effects on phase-advance and firing, therefore, seem to be secondary to the tonic depolarization; i.e., I(h) acts as a tonic leak conductance during locomotion. In the second half of this paper we discuss recent data showing that the neonatal rat spinal cord can produce a stable motor rhythm in the absence of spike activity in premotor interneuronal networks. These coordinated motor neuron oscillations are dependent on NMDA-evoked pacemaker properties, which are synchronized across gap junctions. We discuss the functional relevance for such coordinated oscillations in immature and mature spinal motor systems.
Kiehn
O
O
Section of Neurophysiology, Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark. O.Kiehn@mfi.ku.dk
Kjaerulff
O
O
Tresch
M C
MC
Harris-Warrick
R M
RM
D000818:Animals; D000870:Anterior Horn Cells / Q000187:drug effects / Q000254:growth & development* / Q000502:physiology; D017629:Gap Junctions / Q000187:drug effects / Q000378:metabolism; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D009068:Movement / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D010507:Periodicity; D051381:Rats
D007473:Ion Channels