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Synergistic Regulation of Cytosolic Ca 2+ Concentration in Mouse Astrocytes by NK1 Tachykinin and Adenosine Agonists
Author(s) -
Delumeau Jean C.,
Petitet François,
Cordier Jocelyne,
Glowinski Jacques,
Prémont Joël
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb06418.x
Subject(s) - substance p , chemistry , cytosol , adenosine , agonist , medicine , endocrinology , biophysics , receptor , biochemistry , biology , neuropeptide , enzyme
Abstract The effects on cytosolic Ca 2+ concentration of 2‐chloroadenosine and [L‐Pro 9 ]‐substance P, a selective agonist of NK1 receptors, were investigated on astrocytes from embryonic mice in primary culture. Cells responded to [L‐Pro 9 ]‐ substance P with a transitory increase in cytosolic Ca 2+ which was of shorter duration when external Ca 2+ was removed. A transient response to 2‐chloroadenosine alone occurred. When simultaneously applied, [L‐Pro 9 ]‐substance P and 2‐chloroadenosine evoked a prolonged elevation of cytosolic Ca 2+ (up to 30 min). This phenomenon was dependent on the presence of extracellular Ca 2+ , but insensitive to dihy‐dropyridines, La 3+ , and Co 2+ , excluding the implication of voltage‐operated Ca 2+ channels. Arachidonic acid also induced a sustained elevation of cytosolic Ca 2+ , but did not increase further the response evoked by [L‐Pro 9 ]‐substance P and 2‐chloroadenosine. The activation of protein kinase C by a diacylglycerol analogue mimicked the effect of [L‐Pro 9 ]‐substance P in potentiating the 2‐chloroadenosine‐evoked response. Like 2‐chloroadenosine, pinacidil, which hyper‐polarizes the cells by opening K + channels, prolonged the elevation of cytosolic Ca 2+ concentration induced by [L‐Pro 9 ]‐substance P. Conversely, depolarization with 50 m M KC1 canceled the effects of either pinacidil or 2‐chloroadenosine applied with [L‐Pro 9 ]‐substance P. Pertussis toxin pretreatment suppressed all the effects induced by 2‐chloroadenosine.