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Sodium channels overview

Batrachotoxin at present remains an important, indeed often essential, tool for mechanistic studies of the function of voltage-dependent sodium channels and for the investigation of the role of depolarization and/or influx of sodium ions on physiological functions. Batrachotoxin has been particularly useful in the study of the function of sodium channels, purified and reconstituted into artificial lipid bilayers. A summary and overview of the extensive studies with batrachotoxin appeared in 1986 (5). Since that time more than 100 articles dealing with the activity of batrachotoxin and/ or the radioligand batrachotoxinin A 20a-[ H]benzoate have appeared, and it is beyond the scope of the present review to summarize this extensive recent literature. A few selected developments are as follows allosteric enhancement of the action of batrachotoxins by pyrethroid insecticides... [Pg.191]

Yu, F.H. and Catterall, W.A., Overview of the voltage-gated sodium channel family. Genome Biol, 4, 207, 2003. [Pg.625]

Overview of Insect Voltage-gated Sodium Channels... [Pg.1039]

Figure 4.10. Overview of nerve impulse transmission in chemical synapses. The action potential in the presynaptic nerve cell induces release of the nemotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nicotinic acetylcholine receptor (NAR). The NAR is a hgand-gated channel it will open and become permeable to both and Na. This will move the membrane potential toward the average of the two respective equilibrium potentials however, in the process, the firing level of adjacent voltage-gated sodium charmels will be exceeded, and a full action potential will be triggered (inset). Figure 4.10. Overview of nerve impulse transmission in chemical synapses. The action potential in the presynaptic nerve cell induces release of the nemotransmitter (e.g., acetylcholine) into the synaptic cleft. The transmitter binds to its receptor, e.g. the nicotinic acetylcholine receptor (NAR). The NAR is a hgand-gated channel it will open and become permeable to both and Na. This will move the membrane potential toward the average of the two respective equilibrium potentials however, in the process, the firing level of adjacent voltage-gated sodium charmels will be exceeded, and a full action potential will be triggered (inset).
Figure 6.1. Overview of cellular calcium transport. Calcium enters the cell through voltage- or ligand-gated channels (left). It is extmded by ATP-driven pumps or by sodium antiport (right). Both the mitochondria and the endoplasmic reticulum serve as intracellular calcium stores. The cytosolic concentration is kept at -100 nM under resting conditions. CaM Calmodulin. Figure 6.1. Overview of cellular calcium transport. Calcium enters the cell through voltage- or ligand-gated channels (left). It is extmded by ATP-driven pumps or by sodium antiport (right). Both the mitochondria and the endoplasmic reticulum serve as intracellular calcium stores. The cytosolic concentration is kept at -100 nM under resting conditions. CaM Calmodulin.

See other pages where Sodium channels overview is mentioned: [Pg.464]    [Pg.199]    [Pg.130]   
See also in sourсe #XX -- [ Pg.400 ]




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