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The Case of the OffRhythm Bongo Player

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As explained by Jason Bardi reports from the Scripps Institute, "calcium is a second messenger and regulates many different intracellular processes, including gene expression within cells." (Bardi, 2004) and "the transfer or spread of this excitability to a neuronal network, manifested as electro-graphic and clinical seizures, occurs via synaptic transmission." (Wellmer J, Su H, Beck H, Yaari Y and Eur J Neurosci, 2002) The effect on ion channels and effect on threshold are distinctive in the sense that "native calcium channels have been classified by both their electrophysiological and pharmacological properties and are generally divided into low-threshold (T-types) and high threshold (L-, N-, P/Q- and R-types). The L-, N-, P/Q- and R-type channels typically activate at membrane potentials near -30 mV and display diverse kinetic, voltage-dependent and pharmacological properties.1 The availability of specific pharmacological agents targeting the high threshold channels has permitted elucidation of many of their physiological functions. The T-type calcium channels describe a class of molecules that transiently activate at relatively negative potentials (-60 mV) and for which a general lack of high-affinity selective blockers has made their exact physiological contributions lag behind those of the high-voltage activated isoforms" (Snutch, 2005)
The effect on Bado’s muscles including the aching, twitching and tingling fingers is based on how the calcium mediates constriction and relaxation of blood vessels. This includes those excitable cells which controls the nerve impulses like those occurring in his twitching fingers. More definitively explained by Jane Higdon of the Linus Pauling Institute at Oregon University, calcium
plays a role in mediating the constriction and relaxation of blood vessels (vasoconstriction and vasodilation), nerve impulse transmission, muscle contraction, and the secretion of hormones, such as insulin. Excitable cells, such as skeletal muscle and nerve cells, contain voltage-dependent calcium channels in their cell membranes that allow for rapid changes in calcium concentrations. For example, when a muscle fiber receives a nerve impulse that stimulates it to contract, calcium channels in the cell membrane open to allow a few calcium ions into the muscle cell. These calcium ions bind to activator proteins within the cell that release a flood of calcium ions from storage vesicles inside the cell. The binding of calcium to the protein, troponin-c, initiates a series of steps that lead to muscle contraction. The binding of calcium to the protein, calmodulin, activates enzymes that breakdown muscle glycogen to provide energy for muscle contraction. (Higdon, 2003)
As explained in the following afflictions, cell excitability and effects on the skeletal muscle are discussed:
a) Hyperkalemia: "In acute hyperkalemia, the ratio of intracellular to extracellular K+ is decreased. The gap between the resting membrane potential to the excitability threshold is decreased and the nerve conduction is initiated more easily. If this continues it progresses to weakness of muscles. Gradual hyperkalemia, as in