The Infona portal uses cookies, i.e. strings of text saved by a browser on the user's device. The portal can access those files and use them to remember the user's data, such as their chosen settings (screen view, interface language, etc.), or their login data. By using the Infona portal the user accepts automatic saving and using this information for portal operation purposes. More information on the subject can be found in the Privacy Policy and Terms of Service. By closing this window the user confirms that they have read the information on cookie usage, and they accept the privacy policy and the way cookies are used by the portal. You can change the cookie settings in your browser.
We have studied the possible role of cellular energy status in the regulation of gap junction permeability in rat astrocytes in primary culture. Incubation with the mitochondrial respiratory chain inhibitor antimycin (5 ng/ml) for 16 h caused a significant decrease in ATP concentrations. This effect was accompanied by a dose-dependent inhibition of gap junction permeability as assessed by the scrape-loading/Lucifer yellow transfer technique. No cell death was observed following this treatment. Restoration of cellular ATP levels by a further 24 h incubation in antimycin-free medium reversed the inhibition of Lucifer yellow transfer caused by antimycin. The inhibition of Lucifer yellow transfer brought about by antimycin treatment was also reversed by a short incubation of the cells with the calcium chelator EGTA plus the calcium ionophore A23187. These results suggest that ATP depletion causes a reversible inhibition of gap junction permeability through a calcium-mediated mechanism.