Neurons Say, "Closed Sesame"

Abstract

Astrocytes are often connected by gap junctions. Astrocytes respond to changes in activity of nearby neurons. Rouach et al. cocultured striatal neurons with astrocytes and measured how flux through astrocyte gap junctions was affected by neuronal activity. Simultaneous application of agonists of muscarinic acetylcholine receptors (mAChR) and N -methyl-D-aspartate (NMDA) glutamate receptors inhibited gap junction flux, whereas neither agent affected gap junction communication (GJC) independently. Although the astrocytes express mAChRs, they do not express NMDA receptors. The change in GJC was not due to changes in the expression levels or phosphorylation state of the connexin43 proteins. In cultures of neurons alone or with astrocytes, activation of mAChRs and NMDA receptors promoted the release of arachidonic acid. Pharmacological manipulation of arachidonic availability or production suggested that arachidonic acid was the signaling molecule released from the neurons that inhibited GJC in the astrocytes. Hossain and Boynton describe some of the regulators of connexin43 in an STKE Perspective. N. Rouach. T. Tencé, J. Glowinski, C. Giaume, Costimulation of N -methyl-D-aspartate and muscarinic neuronal receptors modulates gap junctional communication in striatal astrocytes. Proc. Natl. Acad. Sci. U.S.A. 99 , 1023-1028 (2002). [Abstract] [Full Text] M. Z. Hossain, A. L. Boynton, Regulation of Cx43 gap junctions: The gatekeeper and the password. S cience's STKE (2000), [Abstract] [Full Text]