Electrical excitation channels

Voltage-gated Ca2+ channels are Ca2+-selective pores in the plasma membrane of electrically excitable cells, such as neurons, muscle cells, (neuro) endocrine cells, and sensory cells. They open in response to membrane depolarization (e.g., an action potential) and permit the influx of Ca2+ along its electrochemical gradient into the cytoplasm. 

Like other voltage-gated cation channels, Ca2+ channels exist in at least three states A resting state stabilized at negative potentials (such as the resting potentials of most electrically excitable cells) that is a closed state from which the channel can open. The open state is induced by depolarization. Channels do not stay open indefinitely because they are turned off during prolonged depolarization by transition into an inactivated state. Inactivation is driven both by depolarization... 

While many biological molecules may be targets for oxidant stress and free radicals, it is clear that the cell membrane and its associated proteins may be particularly vulnerable. The ability of the cell to control its intracellular ionic environment as well as its ability to maintain a polarized membrane potential and electrical excitability depends on the activity of ion-translocating proteins such as channels, pumps and exchangers. Either direct or indirect disturbances of the activity of these ion translocators must ultimately underlie reperfiision and oxidant stress-induced arrhythmias in the heart. A number of studies have therefore investigated the effects of free radicals and oxidant stress on cellular electrophysiology and the activity of key membrane-bound ion translocating proteins. 

The electrical oscillations at the aqueous-organic interface or at membranes in the absence of any substances relative to the channel or gate were introduced. These oscillations might give some fundamental information on the electrical excitability in living organisms. Since the ion transfer at the aqueous-organic or aqueous-membrane interface and the interfacial adsorption are deeply concerned in the oscillation, it has been stressed that the voltammetry for the ion transfer at an interface of two immiscible electrolyte solutions is... 

H, and Albuquerque, E.X. Interaction of phencyclidine and its analogues on ionic channels of the electrically excitable membrane and nicotinic receptor Implications for behavioral effects. Mai Pharmacol 21 637-647, 1982. 

Albuquerque, E.X. Warnick, J.E. Aguayo, L.G. Ickowicz, R.K. Blaustein, M.P. Maayani, S. and Weinstein, H. Phencyclidine Differentiation of behaviorally active from inactive analogs based on interactions with channels of electrically excitable membranes and of cholinersic receptors. In Kamenka, J.M. Domino, E.F. and Geneste P., eds. Phencvclidine and Related Arvl hexvl ami nes Present and Future Appl i cat ions. Ann Arbor ... 

MYELIN FORMATION, STRUCTURE AND BIOCHEMISTRY 51 MEMBRANE TRANSPORT 73 ELECTRICAL EXCITABILITY AND ION CHANNELS 95 CELL ADHESION MOLECULES 111 THE CYTOSKELETON OF NEURONS AND GLIA 123... 

Taste cells have multiple types of ion channels. TRCs are electrically excitable and capable of generating action-potentials voltage-dependent channels for Na+, Ca2+ and K+, similar to those in neurons, have been detected in vertebrate TRCs. The surface distribution of these channels... 

Aguayo, G., Wamick, J. E., Maayani, S., Glick, S. D., Weinstein, H., and Albuquerque, E. X. (1982) Site of action of phencyclidine. V. Interaction of phencyclidine and its analogues on ionic channels of the electrically excitable membrane and nicotinic receptor Implications for behavioral effects. Mol. Pharmacol., 21 637-647. 

Carbamazepine, valproate, and phenytoin enhance inactivation of voltage-gated sodium and calcium channels and limit the spread of electrical excitation by inhibiting sustained high-frequency firing of neurons. 

Class I— membrane stabilizing drugs to reduce cardiac electrical excitability molecules that are sodium channel blockers, usually based on local anesthetic molecular structure... 

In addition, their ability to stabilize electrically excitable membranes (i.e., quinidine-like properties) through inhibition of fast sodium channels is the action most likely responsible for their most important adverse effects cardiotoxicity and neurotoxicity (410). 

Inhibition of Na fast channels, which can inhibit electrically excitable membranes and produce intracardiac conduction delays ( 137)... 

Because of cocaine s toxicity and addictive properties, a search began for synthetic substitutes for cocaine. In 1905, procaine was synthesized and became the prototypic local anesthetic for half a century. Newer derivatives include mepivacaine and tetracaine (Figure 13.1). Briefly, the SAR of local anesthetics revolves around their hydrophobicity. Association of the drug at hydrophobic sites, such as the sodium channel, is believed to prevent the generation and conductance of a nerve impulse by interfering with sodium permeability (i.e., elevating the threshold for electrical excitability). 

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