THE INHIBITION OF MOTILITY THAT RESULTS FROM CONTACT BETWEEN 2 OLIGODENDROCYTES IN-VITRO CAN BE BLOCKED BY PERTUSSIS TOXIN

The interactions between cultured neonatal rat oligodendrocytes from t he optic nerve were examined. Spontaneous contact between oligodendroc ytes in vitro resulted in collapse of the fine structure of the oligod endrocytes at the points of contact. To increase the frequency of olig odendrocyte-oligodendrocyte interactions, one oligodendrocyte was remo ved from the substrate and placed into contact with the end of a proce ss of another oligodendrocyte. Within 15-30 minutes, the fine structur e of the second oligodendrocyte had collapsed at the point of contact with the manipulated oligodendrocyte. Manipulated contact induced an a pproximately three-fold increase in intracellular free calcium concent ration 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 EG TA. Calcium elevation and contact-induced collapse still occurred in t he absence of extracellular calcium. The contact-induced calcium incre ase was blocked by the combination of EGTA and thapsigargin (to deplet e calcium from IP3 sensitive intracellular storage sites). Pertussis t oxin sensitive G-proteins have been implicated in modulating calcium c hannels and in mediating a release of calcium from internal stores in certain cells. Pertussis toxin prevented the contact-induced calcium i ncrease and the coincident morphological change in oligodendrocytes. T hese results suggest that oligodendrocytes are able to recognize and r eact to specific molecules on the surface of other oligodendrocytes. M oreover, the similarity of this response to the previously characteriz ed response of oligodendrocytes to purified myelin supports the idea t hat molecules present in myelin and exposed on the surfaces of oligode ndrocytes might be used in intercellular communication between oligode ndrocytes. (C) 1996 Wiley-Liss, Inc.