PMID- 11027401 OWN - NLM STAT- MEDLINE DCOM- 20001101 LR - 20190906 IS - 0021-9967 (Print) IS - 0021-9967 (Linking) VI - 426 IP - 4 DP - 2000 Oct 30 TI - Differential regulation of trophic factor receptor mRNAs in spinal motoneurons after sciatic nerve transection and ventral root avulsion in the rat. PG - 587-601 AB - After sciatic nerve lesion in the adult rat, motoneurons survive and regenerate, whereas the same lesion in the neonatal animal or an avulsion of ventral roots from the spinal cord in adults induces extensive cell death among lesioned motoneurons with limited or no axon regeneration. A number of substances with neurotrophic effects have been shown to increase survival of motoneurons in vivo and in vitro. Here we have used semiquantitative in situ hybridization histochemistry to detect the regulation in motoneurons of mRNAs for receptors to ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), glial cell line-derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) 1-42 days after the described three types of axon injury. After all types of injury, the mRNAs for GDNF receptors (GFRalpha-1 and c-RET) and the LIF receptor LIFR were distinctly (up to 300%) up-regulated in motoneurons. The CNTF receptor CNTFRalpha mRNA displayed only small changes, whereas the mRNA for membrane glycoprotein 130 (gp130), which is a critical receptor component for LIF and CNTF transduction, was profoundly down-regulated in motoneurons after ventral root avulsion. The BDNF full-length receptor trkB mRNA was up-regulated acutely after adult sciatic nerve lesion, whereas after ventral root avulsion trkB was down-regulated. The NT-3 receptor trkC mRNA was strongly down-regulated after ventral root avulsion. The results demonstrate that removal of peripheral nerve tissue from proximally lesioned motor axons induces profound down-regulations of mRNAs for critical components of receptors for CNTF, LIF, and NT-3 in affected motoneurons, but GDNF receptor mRNAs are up-regulated in the same situation. These results should be considered in relation to the extensive cell death among motoneurons after ventral root avulsion and should also be important for the design of therapeutical approaches in cases of motoneuron death. CI - Copyright 2000 Wiley-Liss, Inc. FAU - Hammarberg, H AU - Hammarberg H AD - Department of Neuroscience, Nobels v. 12A, Karolinska Institute, S-171 77 Stockholm, Sweden. Henrik.Hammarberg@neuro.ki.se FAU - Piehl, F AU - Piehl F FAU - Risling, M AU - Risling M FAU - Cullheim, S AU - Cullheim S LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Comp Neurol JT - The Journal of comparative neurology JID - 0406041 RN - 0 (RNA, Messenger) RN - 0 (Receptors, Growth Factor) SB - IM MH - Aging/metabolism MH - Animals MH - Animals, Newborn/growth & development/metabolism/physiology MH - *Axotomy/methods MH - Cell Survival/physiology MH - Denervation MH - Motor Neurons/*metabolism MH - Nerve Regeneration/physiology MH - RNA, Messenger/*metabolism MH - Rats/*metabolism MH - Rats, Sprague-Dawley MH - Receptors, Growth Factor/*genetics MH - Reference Values MH - Sciatic Nerve/physiology MH - Spinal Cord/cytology/*metabolism MH - Spinal Nerve Roots/injuries/physiology MH - Up-Regulation MH - Wounds and Injuries/metabolism EDAT- 2000/10/12 11:00 MHDA- 2001/02/28 10:01 CRDT- 2000/10/12 11:00 PHST- 2000/10/12 11:00 [pubmed] PHST- 2001/02/28 10:01 [medline] PHST- 2000/10/12 11:00 [entrez] AID - 10.1002/1096-9861(20001030)426:4<587::AID-CNE7>3.0.CO;2-R [pii] AID - 10.1002/1096-9861(20001030)426:4<587::aid-cne7>3.0.co;2-r [doi] PST - ppublish SO - J Comp Neurol. 2000 Oct 30;426(4):587-601. doi: 10.1002/1096-9861(20001030)426:4<587::aid-cne7>3.0.co;2-r.