Operantly conditioned motoneuron plasticity: possible role of sodium channels.
1. Learning is traditionally thought to depend on synaptic plasticity. However, recent work shows that operantly conditioned decrease in the primate H reflex is associated with an increase in the depolarization needed to fire the spinal motoneuron (VDEP) and a decrease in its conduction velocity (CV). Furthermore, the increase in VDEP appears to be largely responsible for the H-reflex decrease. The conjunction of these changes in VDEP and CV suggests that an alteration in Na+ channel properties throughout the soma and axon could be responsible. 2. A mathematical model of the mammalian myelinated axon was used to test whether a positive shift in the voltage dependence of Na+ channel activation, a decrease in Na+ channel peak permeability, or changes in other fiber properties could have accounted for the experimental findings. 3. A positive shift of 2.2 mV in Na+ channel activation reproduced the experimentally observed changes in VDEP and CV, whereas a reduction in Na+ channel permeability or changes in other fiber properties did not. 4. These results are consistent with the hypothesis that operantly conditioned decrease in the primate H reflex is largely due to a positive shift in the voltage dependence of Na+ channel activation. Recent studies suggest that change in activation of protein kinase C may mediate this effect.
Halter
J A
JA
Division of Restorative Neurology and Human Neurobiology, Baylor College of Medicine, Houston, Texas 77030, USA.
Carp
J S
JS
Wolpaw
J R
JR
D000200:Action Potentials; D000818:Animals; D003216:Conditioning, Operant; D006801:Humans; D008959:Models, Neurological; D009046:Motor Neurons / Q000502:physiology*; D009473:Neuronal Plasticity; D015222:Sodium Channels / Q000502:physiology*
D015222:Sodium Channels