The inhibition of motility that results from contact between two oligodendrocytes in vitro can be blocked by pertussis toxin

The interactions between cultured neonatal rat oligodendrocytes from the optic nerve were examined. Spontaneous contact between oligodendrocytes in vitro resulted in collapse of the fine structure of the oligodendrocytes at the points of contact. To increase the frequency of oligodendrocyte-oligodendrocyte interactions, one oligodendrocyte was removed from the substrate and placed into contact with the end of a process of another oligodendrocyte. Within 15–30 minutes, the fine structure of the second oligodendrocyte had collapsed at the point of contact with the manipulated oligodendrocyte. Manipulated contact induced an approximately three-fold increase in intracellular free calcium concentration that preceded the inhibition of motility. To demonstrate that a release of calcium from internal stores was involved, the experiment was repeated with calcium removed from the medium by chelation with EGTA. Calcium elevation and contact-induced collapse still occurred in the absence of extracellular calcium. The contact-induced calcium increase was blocked by the combination of EGTA and thapsigargin (to deplete calcium from IP3 sensitive intracellular storage sites). Pertussis toxin sensitive G-proteins have been implicated in modulating calcium channels and in mediating a release of calcium from internal stores in certain cells. Pertussis toxin prevented the contact-induced calcium increase and the coincident morphological change in oligodendrocytes. These results suggest that oligodendrocytes are able to recognize and react to specific molecules on the surface of other oligodendrocytes. Moreover, the similarity of this response to the previously characterized response of oligodendrocytes to purified myelin supports the idea that molecules present in myelin and exposed on the surfaces of oligodendrocytes might be used in intercellular communication between oligodendrocytes. © 1996 Wiley-Liss, Inc.