Expression of CHL1 and L1 by neurons and glia following sciatic nerve and dorsal root injury

Cell adhesion molecules (CAMs), particularly L1, are important for axonal g rowth on Schwann cells in vitro. We have used in situ hybridization to stud y the expression of mRNAs for L1 and its close homologue CHL1, by neurons r egenerating their axons in vivo, and have compared CAM expression with that of GAP-43. Adult rat sciatic nerves were crushed (allowing functional rege neration), or cut and ligated to maintain axonal sprouting but prevent reco nnection with targets. In other animals lumbar dorsal roots were transected to produce slow regeneration of the central axons of sensory neurons. In u noperated animals L1 and CHL1 mRNAs were expressed at moderate levels by sm all- to medium-sized sensory neurons and L1 mRNA was expressed at moderate levels by motor neurons. Many large sensory neurons expressed neither L1 no r CHL1 mRNAs and motor neurons expressed little or no CHL1 mRNA. Neither mo tor nor sensory neurons showed any obvious upregulation of L1 mRNA after ax otomy. Increased CHL1 mRNA was found in motor neurons and small- to medium- sized sensory neurons 3 days to 2 weeks following sciatic nerve crush, decl ining toward control levels by 5 weeks when regeneration was complete. Cut and ligation injuries caused a prolonged upregulation of CHL1 mRNA(and GAP- 43 mRNA), indicating that reconnection with target tissues may be required to signal the return to control levels. Large sensory neurons did not upreg ulate CHL1 mRNA after axotomy and thus regenerated within the sciatic nerve without producing CHL1 or L1. Dorsal root injuries caused a modest, slow u pregulation of CHL1 mRNA by some sensory neurons. CHL1 mRNA was also up-reg ulated by many presumptive Schwann cells in injured nerves and by some sate llite cells around large sensory neurons after sciatic nerve injuries and w as transiently upregulated by some astrocytes in the degenerating dorsal co lumns after dorsal rhizotomy.