By Robert A. Maue (Eds.)
Covers a extensive spectrum of knowledge rising from households of ion channels and provides new new viewpoints at the vital periods of those channels. Highlights situations the place the functionality and disorder of channel molecules have furthered knowing of the body structure and pathophysiology of cells tissues and organs. plentiful illustrations. For researchers.
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Additional info for Molecular Insights into Ion Channel Biology in Health and Disease
Leao and H. von Gersdorff, personal communication). It is thought that this rapid gating allows fast conduction and subsequent comparison of the time of arrival of sounds in one ear versus the other, thus allowing sounds to be located in space. 2. Differences in gating among sodium channel isoforms Are the unusual properties of sodium currents in the two above examples due to the unique functional characteristics of individual isoforms? Alternatively, are they caused by cellular modifications to the “stereotypic” manner in which all sodium channels gate, or could they be due to a combination of these two mechanisms?
Overall, it appears likely from these three examples that sodium channel isoforms serve unique functions. Within the past ten years many single amino acid mutations in the skeletal muscle sodium channel have been identified that produce skeletal muscle diseases, especially the periodic paralyses (hyperkalemic periodic paralysis, paramyotonia congenita, and some forms of hypokalemic periodic paralysis ; reviewed recently by Lehmann-Horn et al. ). Mutations of the cardiac sodium channel are responsible for some cases of long Q –T syndrome, a cause of sudden cardiac arrest.
Most of the identified mutations in muscle and neuronal sodium channels lie in three general regions: the transmembrane domains (especially domains III and IV), the regions close to the membrane, or the cytoplasmic domain that is important for fast inactivation (the III– IV linker). It is highly likely that deleterious but nonlethal mutations occur in the large intracellular or extracellular domains and that these mutations interfere with channel targeting and/or modulation (see Fig. 11). Finally, now that detailed information is accruing regarding the functional diversity among sodium channel isoforms and its differential regulation, it becomes essential that this diversity be studied in the context of meaningful biological roles.