Mojave Toxin: A Selective Ca(++) Channel Antagonist

Mojave toxin, the principal toxic component of the venom of the Mojave rattlesnake, is a protein complex of 22,000 daltons. The mechanism of this potent neurotoxin is unclear, but physiologic data suggest an action on ion channels. The specificity of Mojave toxin for receptors associated with Calciu...

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Bibliographische Detailangaben
Hauptverfasser:	Valdes, James J, Wolff, Vicki L, Menking, Darrel E, Thompson, Roy G, Chambers, James P
Format:	Report
Sprache:	eng
Schlagworte:	BRAIN CALCIUM CALCIUM CHANNELS CHANNELS CHLORINE CNS DEPRESSANTS ION CHANNELS IONS LIGANDS LPN-DA-21083000B134 MOJAVE RATTLESNAKES MOJAVE TOXIN NERVE TRANSMISSION NERVES NEUROCHEMICAL TRANSMISSION NEUROTOXINS ORGANS(ANATOMY) Pharmacology PHYSIOLOGY POTENCY RATS SHARKS SODIUM TOXICITY Toxicology TOXINS AND ANTITOXINS VENOMS
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Zusammenfassung:	Mojave toxin, the principal toxic component of the venom of the Mojave rattlesnake, is a protein complex of 22,000 daltons. The mechanism of this potent neurotoxin is unclear, but physiologic data suggest an action on ion channels. The specificity of Mojave toxin for receptors associated with Calcium (++), Chlorine (-1), and Sodium (+) channels was assessed using a competitive binding paradigm. Mojave toxin competitively and irreversibly inhibits binding to dihydropyridine receptors associated with neuronal Ca(++) channels but had no effect on C1(-) and na(+) channels. The pharmacologic specificity of Mojave toxin makes it a useful probe of Ca(++) channel function. Keywords: Brain, Rats, Sharks, Electric organ, Nerves, Nerve transmission, Ligands. Prepared in collaberation with Texas Univ., San Antonio.