Variable mechanisms of action of lithium during generating of membrane potential oscilations across the excitable membrane of the Nitela cell

This study presents results on variable mechanisms of lithium transport processes during generating of membrane potential oscillations across the very excitable membrane of the Nittela cell. Generating of several classes of oscillations, single and local impulses of the membrane potential, were presented in dependence on effects of a high LiCl concentration (10 mM), with which the cell membrane is very excited. Results on membrane potential oscillations are presented, and then some of oscillogram parameters were displayed. The assertion is that oscillations of the membrane potential are caused by total oscillatory transport processes: Li+, K+, Na+ and Cl-across the very excitable cell membrane. The paper presents the hypothesis on mechanisms of oscillatory transport processes of ions (Li, Na, K and Cl) expressed over different classes of oscillations, single and local impulses of the membrane potential across the excitable membrane of the Nittela cell.

Calpain Inhibitors Alter the Excitable Membrane Properties of Cultured Aplysia Neurons

The calpain superfamily of calcium-dependent papain-like cysteine proteases constitutes highly conserved proteases that function to posttranslationally modify substrates by partial proteolysis. Calpains are known to proteolyze >100 substrates that lack strong sequence homology. Consequently, the calpain superfamily has been implicated in playing a central role in diverse physiological and pathological processes. Investigation of the physiological functions of calpains, on the one hand, and the need to develop pharmacological reagents to inhibit calpain-mediated pathological processes, on the other hand, led to the development of numerous calpain inhibitors. Using cultured Aplysia neurons and voltage-clamp analysis, we report here that the calpain inhibitors calpeptin, MG132, and the calpain inhibitor XII inhibit voltage-gated potassium conductance and moderately reduce the sodium conductance. These consequently lead to spike broadening and increased calcium influx. Such alterations of the excitable membrane properties may alter the normal patterns of neuronal and muscle electrical activities and thus should be taken into account when evaluating the effects of calpain inhibitors as protective/therapeutic drugs and as research tools.