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When adult nerves were transected to cause permanent axotomy, previously myelinating Schwann cells expressed progressively more GAP\u201043\u2010immunoreactivity over 3 weeks and GAP\u201043 mRNA levels increased over a similar time course. The peak level of GAP\u201043 mRNA occurred at least 2 weeks later than that of nerve growth factor receptor, another marker of denervated Schwann cells. In contrast, after nerve\u2010crush, which allows axonal regeneration, many fewer Schwann cells had GAP\u201043\u2010immunoreactivity, and the amount of GAP\u201043 mRNA was markedly lower than in transected nerves. Forskolin, a drug that activates adenylate cyclase and mimics many effects of axon\u2010Schwann cell interactions, markedly reduced GAP\u201043\u2010immunoreactivity and mRNA expression in cultured Schwann cells, whereas interleukin\u20101 had no effect. These data demonstrate that axon\u2010Schwann cell interactions inhibit the expression of GAP\u201043 in Schwann cells and that this effect is mimicked by forskolin. \u00a9 1994 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.490380510","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T02:00:55Z","timestamp":1104544855000},"page":"575-589","source":"Crossref","is-referenced-by-count":47,"title":["Expression of growth\u2010associated protein\u201043 kD in Schwann cells is regulated by axon\u2010Schwann cell interactions and cAMP"],"prefix":"10.1002","volume":"38","author":[{"given":"S. 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