Annals of the New York Academy of Sciences
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Ann. N. Y. Acad. Sci. · Jan 1991
ReviewRole of signal transduction in anesthetic action. Alpha 2 adrenergic agonists.
The molecular mechanism for general anesthetic action is not known. The alpha 2 adrenergic agonists represent a novel class of "anesthetic-like" agent because of their selectivity for receptor binding sites and because the transmembrane signaling systems mediating their biologic responses in non-CNS systems are known. We have begun to characterize the signal transduction pathway involved in the anesthetic-like action of the alpha 2 adrenergic agonists. ⋯ Subsequently, data using molecular biologic techniques suggested that the alpha 2 C4 isoreceptor was the probable receptor that mediated the anesthetic response. We further explored the postreceptor effector mechanism for the signal transduction pathway for alpha 2 anesthetic action and identified the participation of two other molecular components, namely, a pertussis-toxin-sensitive G protein and a 4-aminopyridine-sensitive ion channel. Whether the signal transduction pathway for alpha 2 anesthetic action mediates the further response to other non-alpha 2 anesthetic agents needs to be defined.
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Ann. N. Y. Acad. Sci. · Jan 1991
ReviewSaturable binding of anesthetics to nicotinic acetylcholine receptors. A possible mechanism of anesthetic action.
Recent controversies in the existence of saturable binding of general anesthetics in brain tissues prompted a careful examination of specific binding of anesthetics to neural receptors. We examined the binding of both local and general anesthetics using electron spin resonance and radioligand criteria. ⋯ Association of anesthetic at this crevice is in turn dependent on the anesthetic concentration in the lipid phase of the membrane. The hypothesis provides a mechanism for the saturable interaction of anesthetics with their protein target site in the membrane without violating the correlations expressed by the Meyer-Overton rule of anesthetic action.
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Ann. N. Y. Acad. Sci. · Jan 1988
ReviewMechanisms of virus-induced demyelination and remyelination.
Viral models of demyelination and remyelination provide important clues to the pathogenesis of multiple sclerosis. Determining the precise viral polypeptides recognized by T cells during the demyelinating process will be important in understanding the mechanisms of viral-induced myelin destruction. Isolation, purification, and characterization of factors that promote remyelination and proliferation of oligodendrocytes may provide hope in the treatment of patients with chronic demyelinating disorders.