@article {2121,
	title = {Vortex shedding as a precursor of turbulent electrical activity in cardiac muscle.},
	journal = {Biophys J},
	volume = {70},
	year = {1996},
	month = {03/1996},
	pages = {1105-11},
	abstract = {<p><span style="font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;">In cardiac tissue, during partial blockade of the membrane sodium channels, or at high frequencies of excitation, inexcitable obstacles with sharp edges may destabilize the propagation of electrical excitation waves, causing the formation of self-sustained vortices and turbulent cardiac electrical activity. The formation of such vortices, which visually resembles vortex shedding in hydrodynamic turbulent flows, was observed in sheep epicardial tissue using voltage-sensitive dyes in combination with video-imaging techniques. Vortex shedding is a potential mechanism leading to the spontaneous initiation of uncontrolled high-frequency excitation of the heart.</span></p>},
	keywords = {Animals, Biophysical Phenomena, Biophysics, Cell Membrane, Computer Simulation, Electric Stimulation, Electrochemistry, Electrophysiology, Heart, Models, Cardiovascular, Myocardial Contraction, Myocardium, Sheep, Sodium Channels},
	issn = {0006-3495},
	doi = {10.1016/S0006-3495(96)79691-1},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/8785270},
	author = {Cabo, C and Pertsov, A V and Davidenko, J M and Baxter, Bill and Gray, R A and Jalife, J}
}
@article {3166,
	title = {Operantly conditioned motoneuron plasticity: possible role of sodium channels.},
	journal = {Journal of neurophysiology},
	volume = {73},
	year = {1995},
	month = {02/1995},
	pages = {867{\textendash}871},
	abstract = {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.},
	keywords = {Sodium Channels},
	issn = {0022-3077},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/7760141},
	author = {Halter, J. A. and Jonathan S. Carp and Jonathan Wolpaw}
}
