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Pertussis toxin (PTx) inactivated an OEC G<jats:sub>i\/o<\/jats:sub> protein as pretreating OECs with the PTx B\u2010oligomer subunit had no effect on RGC neurite regrowth. However, the B\u2010oligomer was responsible for decreasing the marked orientation of neurite regrowth on the OEC substrate. Simultaneous incubation of OECs with PTx and a depolarizing concentration of KCl abolished the increase in neurite regrowth from cocultured RGCs, but exposure to a depolarizing KCl concentration after OECs had been PTx\u2010treated had no effect. Our evidence supports the hypothesis that G\u2010protein\u2010regulated calcium signaling plays a significant role in OEC support for CNS axonal regeneration. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.10299","type":"journal-article","created":{"date-parts":[[2003,11,3]],"date-time":"2003-11-03T08:01:42Z","timestamp":1067846502000},"page":"232-241","source":"Crossref","is-referenced-by-count":13,"title":["Manipulation of olfactory ensheathing cell signaling 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