Protective Effect Of GDNF On Spinal Cord Motorneuron In Incomplete SCI And Its Mechanism In Rat

ln near two decades, it has been proved that central neurons have the ability ofplasticity and regenerating, which could be enhanced by applying neurotrophics. lthas been becoming a "hot dot" for neurotrohpics to maintain the development ofneurons and rescue the injuried neurons. Glial cell line-derived neurotrophic factor(GDNF) is a neurotrophic polypeptide, distantly related to transforming growthfactorbeta (TGF-beta), originally isolated by virtue of its ability to induce dopamineuptake and cell survival in cultures of embryonic ventral midbrain dopaminergicneurons, and more recently shown to be a potent neurotrophic factor for motorneurons.But the bioIogical activities and the expression of GDNF at injuried spinalmotorneuron in vivo presently unknown. So those was observed in this study througha modefied Allen's spinal injury model.The main resuIts of our research are as follows:l. The RT-PCR showed that the expression of GDNFmRNA at spinal cord segmentelevated notablely at 24, 72 and l68 hours after SCl in contrast to normal, and theexpression peak at 72 hours postoperatively.2. The result of Tarlov grading and Rivlin's incline plate for testing spinal functionindicated that GDNF could improve markedly motor function of hind limbs.3. Motor evoked potential(MEP) and somatosensory evoked potential(SEP) showedthe incubation was prolonged and the amplitude was reduced at 3, 7 and l4 daysafter SCI. The spinal cord signal of the MEP was more sensitive to injury than theSEP,but the SEP retUrn earlier after injury than the MEP lt should accelerate therecovery of the shape and incubation of the evoked potential for GPNF to be usedlocally through subarachnoid.4. EnZyme histochemistry was used to show CHE and ACP activity of spinal3motoneurons in spinal segnents combined With mp ~ ~ni-by Vitheof mean grey(MG) and effective diameter(ED). The activity of CHE which wasweaken as SCI could be obviously increased at 7 and l0 days after SCI. Theactivity Qf ACP could be cut dQwn for the use of GDM which had been highlyimproved by reason of SCI. Exogenous GDwe protects notorneurons from SCI.5. The cycosolic Ca2+ in the spinal cord segment increased at 24 hours and peaked at72 hours after SCI. GDNF could slacken this tendency and there was a positivecorrelation between them. Those suggest it should be a possible mechanic forW to proteCt motomeurons from secondary SCI and improve spinal fiJnction.