Gating mechanisms calcium channels

Collectively, the in situ biochemical evidence suggests that voltage-gated calcium channels are modified by pyrethroids however, the mechanism by which Types I and II pyrethroids accomplish this may be different. Specifically, Type II pyrethroids are more potent enhancers of calcium influx and glutamate release under depolarizing conditions than Type I pyrethroids and may contribute, in part, to different symptoms elicited by these classes of pyrethroids in vivo. 

Hoth, M., Button, D. C. and Lewis, R. S., 2000, Mitochondrial control of calcium-channel gating a mechanism for sustained signaling and transcriptional activation in T lymphocytes. Proc Natl Acad Sci U 5 A 97, 10607-12. 

In the myocardium, automaticity is the ability of the cardiac muscle to depolarize spontaneously (i.e., without external electrical stimulation from the autonomic nervous system). This spontaneous depolarization is due to the plasma membrane within the heart that has reduced permeability to potassium (K+) but still allows passive transfer of calcium ions, allowing a net charge to build. Automaticity is most often demonstrated in the sinoatrial (SA) node, the so-called pacemaker cells. Abnormalities in automaticity result in rhythm changes. The mechanism of automaticity involves the pacemaker channels of the HCN (Hyperpolarization-activated, Cyclic Nucleotide-gated) family14 (e.g., If, "funny" current). These poorly selective cation channels conduct more current as the membrane potential becomes more negative, or hyperpolarized. They conduct both potassium and sodium ions. The activity of these channels in the SA node cells causes the membrane potential to slowly become more positive (depolarized) until, eventually, calcium channels are activated and an action potential is initiated. 

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