Τόμος 20 (2006) – Τεύχος 2 – Άρθρο 47 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Διεθνής Έκδοση – Volume 20 (2006) – Issue 2 – Article 47 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-International Edition

Title TGF-b expression in the neonatal rat spinal cord after sciatic nerve injury
Authors D. Kapoukranidou, B. Michailidou, A. Kritis and M. Albani

Department of Physiology and Pharmakology, Medical School, Aristotle University, Thessaloniki, Greece

Citation Kapoukranidou, D., Michailidou, B., Kritis, A., Albani, M.: TGF-b expression in the neonatal rat spinal cord after sciatic nerve injury, Epitheorese Klin. Farmakol. Farmakokinet. 20(2): 192-194 (2006)
Publication Date Accepted for publication: 19-20 May 2006
Full Text Language English
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Keywords TGF-b, axotomy, motoneuron, immunochemistry.
Other Terms review article
Summary Sciatic nerve injury in the neonatal rat leads to motoneuron degeneration through mechanisms that are not fully understood yet. Various factors are implicated in this procedure among which, a multifunctional cytokine, the TGF-b. In this essay, we studied the possible changes in TGF-b expression in the neonatal rat spinal cord after unilateral sciatic nerve injury. A sciatic nerve injury was caused by a forceps on 7 days old wistar rats. The rats were sacrificed and their spinal cords were removed on 12, 24, 48, 72 hours, 1 week and 1 month, following nerve injury. Cryostat sections 0,4µ were taken and immunostaining was carried out using an anti-TGF-b1 antibody. TGF-b immunostaining was observed within spinal cord motoneurons of the 12 hour group and the 1 month group after axotomy, while in the rest of the groups there was no difference between controls and operated animals. No TGF-b immunostaining was observed in any of the controls. Our findings agree with the existing literature that TGF-b expression is increased as a result to injury, and thus support the theory of its neuroprotective action. Nevertheless, the relevant mechanisms of action still remain unclear.
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