The cell recognition molecule CHL1 is strongly upregulated by injured and regenerating thalamic neurons

Close homologue of L1 (CHL1) is a cell recognition molecule known to promot e axonal growth in vitro. We have investigated the expression of CHL1 mRNA by regenerating central nervous system (CNS) neurons, by using in situ hybr idisation 3 days to 10 weeks following the implantation of living and freez e-killed peripheral nerve autografts into the thalamus of adult rats. At al l survival times after implantation of living grafts, neurons of the thalam ic reticular nucleus (TRN), close to the graft tip and up to 1 mm away from it, displayed strong signal for CHL1 mRNA, even though TRN neurons show ve ry low levels of CHL1 mRNA expression in unoperated animals. When the cell bodies of regenerating neurons were identified by retrograde labelling from the distal portion of the grafts, 4-6 weeks after operation, most Of the l abelled cells were found in the TRN and could be shown to have upregulated CHL1 mRNA. In addition, some neurons in dorsal thalamic nuclei near the gra ft tip transiently upregulated CHL1 mRNA during the first 3 weeks after gra ft implantation, and glial cells showing CHL1 mRNA expression were present at the brain/graft interface 3 days to 2 weeks after operation. Freeze-kill ed grafts, into which axons do not regenerate, caused a transient upregulat ion of CHL1 in very few TRN neurons near the graft tip and in glial cells a t the brain/graft interface but did not produce prolonged CHL1 mRNA express ion. CHL1 can therefore be added to the List of molecules (including CAP-43 , L1, and c-jun) strongly expressed by CNS neurons that regenerate their ax ons into nerve grafts, but not by those neurons that fail to regenerate the ir axons. J. Comp. Neurol. 425:382-392, 2000. (C) 2000 Wiley-Liss, Inc.