Differential effects of propofol and ketamine on cytosolic calcium concentrations of astrocytes in primary culture.

Abstract

Propofol has been shown recently to alter cellular communication mediated by gap junctions between astrocytes (a glial cell subpopulation involved in major brain functions). As marked increases in concentrations of cytosolic calcium ([Ca2+]i) produce closure of the gap junction, we have investigated the effects of both propofol and ketamine on resting [Ca2+]i concentrations in mouse cultured astrocytes using microfluorimetry with the indo-1 fluorescent probe. Propofol 10(-5) and 10(-4) mol litre-1 induced a monophasic transitory Ca2+ peak in a large subpopulation of the cells tested. This response exhibited characteristics close to those of the peak elicited by [L-Pro9] substance P (10(-7) mol litre-1), an activator of phospholipase C in astrocytes. In both cases, it possibly corresponded to mobilization of Ca2+ from endogenous stores. In a few cases, however, administration of propofol induced a moderate, but sustained increase in [Ca2+]i corresponding to the entry of external Ca2+ into the cells. In contrast, ketamine 10(-5) and 10(-4) mol litre-1 failed to affect [Ca2+]i resting concentrations. These findings indicate that clinically relevant concentrations of propofol, but not ketamine, increased [Ca2+]i concentration in astrocytes.