01900nas a2200181   4500008004100000022001400041245008300055210006900138260001200207300001400219490000700233520134800240653002001588100001901608700002301627700002101650856004701671       1995                        eng d  a0022-307700aOperantly conditioned motoneuron plasticity: possible role of sodium channels.0 aOperantly conditioned motoneuron plasticity possible role of sod  c02/1995  a867–8710 v733 a1. 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.10aSodium Channels1 aHalter, J., A.1 aCarp, Jonathan, S.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/7760141