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PubMed1993

Molecular cloning, functional properties, and distribution of rat brain alpha 7: a nicotinic cation channel highly permeable to calcium.

A full-length clone coding for the rat alpha 7 nicotinic receptor subunit was isolated from an adult brain cDNA library and expressed in Xenopus oocytes. A significant proportion of the current through alpha 7-channels is carried by Ca2+. This Ca2+ influx then activates a Ca(2+)-dependent Cl- conductance, which is blocked by the chloride channel blockers niflumic and fluflenamic acid. Increasing the external NaCl concentration caused the reversal potentials for the alpha 7-channels and the Ca(2+)-dependent Cl- channels to be shifted in opposite directions. Under these conditions, agonist application activates a biphasic current with an initial inward current through alpha 7-channels followed by a niflumic acid- and fluflenamic acid-blockable outward current through Ca(2+)-dependent Cl- channels. A relative measure of the Ca2+ permeability was made by measuring the shift in the reversal potential caused by adding 10 mM Ca2+ to the external solution. Measurements made in the absence of Cl-, to avoid artifactual current through Ca(2+)-activated Cl- channels, indicate that alpha 7-homooligomeric channels have a greater relative Ca2+ permeability than the other nicotinic ACh receptors. Furthermore, alpha 7-channels have an even greater relative Ca2+ permeability than the NMDA subtype of glutamate receptors. High levels of alpha 7-transcripts were localized by in situ hybridization in the olfactory areas, the hippocampus, the hypothalamus, the amygdala, and the cerebral cortex. These results imply that alpha 7-containing receptors may play a role in activating calcium-dependent mechanisms in specific neuronal populations of the adult rat limbic system.

Amino Acid Sequence↗
PubMed1980

Augmentation of allergic histamine release from human leukocytes by nonsteroidal anti-inflammatory-analgesic agents.

Augmentation of allergic histamine release in vitro with human leukocytes was produced by numerous nonsteroidal anti-inflammatory--analgesic agents, primarily the arylalkanoic and anthranilic acids. Augmentation occurred without release of histamine by the agents in the absence of the allergen (ragweed) and only under conditions of an accompanying release by the allergen. As a consequence of augmentation, less allergen was necessary to produce a given response in the presence of these agents. It is suggested that some of these agents might enhance mediator release in immediate-type hypersensitivity reactions. The same agents reported to exacerbate chronic urticaria, i.e., indomethacin, mefenamic acid, sodium salicylate, aspirin, sodium benzoate, and tartrazine, also augmented allergic histamine release. Pharmacologically mediated augmentation of mediator release from stimulated cells is suggested to be involved in the exacerbation of existing chronic urticaria by the acidic nonsteroidal anti-inflammatory-analgesic agents.

Adult↗