Search

Objective: To investigate the effect of exogenous glial cell line-derived neurotrophic factor (GDNF) infused into the cavitas subarachnoidealis on cornu anterius medullae spinalis motor neurons after sciatic nerve axotomy., Methods: Forty-eight healthy SD rats were divided into 2 groups randomly: GDNF group and NS group. The left sciatic nerve in rats were cut off. And then 0.9% saline (6 microl) and GDNF solution (6 microl) were injected into cavitas subarachnoidealis at L4-L6 in NS group and GDNF group,respectively. The rats were sacrificed on postoperative 1, 2, 4 and 8 weeks respectively. Their specimen of L4-L6 spinal cord were taken at different time and sectioned. The HE staining, Nissl staining and cholinesterase (ChE) staining in motor neurons were used for counting of motor neurons., Results: In GDNF group the number of motor neurons in cornu anterius medullae spinalis and the ChE activity were higher than that of NS group., Conclusion: The exogenous GDNF infused into the cavitas subarachnoidealis are supposed to protect the degenerated spinal motor neuron from death after sciatic nerve injury.

The aim of this study was to investigate the protective effect of exogenous bcl-2 on spinal cord motoneurons following sciatic nerve axotomy. After epineurium suturing, sense bcl-2 (Ad/s-bcl-2), antisense bcl-2 (Ad/as-bcl-2), or reporter gene lacZ (Ad/lacZ) recombinant adenovirus or NS was injected into the sciatic nerve 0.5 cm distant from the sutured point respectively in different groups. The rats were transcardially perfused with 4% paraformaldehyde on postoperative 48 h, 7 d, 15 d and 30 d respectively and the spinal cords of L4 to L6 were harvested. X-gal staining, bcl-2 in situ hybridization and immunohistochemical staining, TUNEL (terminal deoxynucleotidyl transferase mediated dUTP nick end labeling) staining and AChE (acetyl cholinesterase) histochemical staining were used. We observed that the exogenous lacZ gene was expressed in the spinal cord of Ad/lacZ group, and sense bcl-2 significantly decreased the number of apoptotic motoneurons and the decreasing degree of AChE activity of the motoneurons in the spinal cord induced by sciatic nerve axotomy and accelerate AChE activity recovery. However, antisense bcl-2 increased the number of apoptotic motoneurons and the decreasing degree of AChE activity of the motoneurons in the spinal cord induced by sciatic nerve axotomy and prolonged AChE activity recovery. These results demonstrate that exogenous bcl-2 may protect motor neurons from injury induced by peripheral nerve axotomy.

We focus on how peripheral nerves or their tissue constituents including Schwann cells, fibroblasts and neurotrophic factors are used to overcome the unfavorable extrinsic CNS environment and upregulate the intrinsic growth potential of injured neurons for the enhancement of neuronal survival and axonal regeneration of axotomized retinal ganglion cells in adult mammals.

Objective: To study the expression and distribution of brain derived neurotrophic factor (BDNF) and fibroblast growth factor-2 (FGF-2) in normal facial motoneurons (FMNs) and in FMNs following axotomy., Methods: The right facial nerves were transected 6 mm distal to the stylomastoid foraman in adult Wistar rats except the normal group. Serial 20 microns cryosections were cut through the whole brainstems. Expressions of BDNF and FGF-2 mRNA as well as BDNF and FGF-2 protein were studied by in situ hybridization, immunohistochemistry and image analysis., Results: BDNF mRNA and its protein were observed in widespread areas of normal rat facial nucleus, and those increased 1 day after axotomy. In addition to neurons, glial cells were also stained. FGF-2 mRNA and its protein were mainly localized in normal FMNs of ventral facial nucleus. After axotomy, expression of FGF-2 mRNA started to up-regulate in FMNs at 7 days, however FGF-2 protein drastically reduced at 3 and 7 days., Conclusion: In addition to target-supporting, there may be BDNF autocrine and paracrine mechanisms as well as FGF-2 autocrine mechanisms in normal rat FMN. When target-derived BDNF is deprived, alternative sources of BDNF support may substitute immediately after axotomy. However, deprivating of target--derived FGF-2 may result in down-regulation of FGF-2 protein in adult rat FMNs at early stage after axotomy. These suggest that the exogenous FGF-2 might provide a supportive environment for the recovery of metabolism and function of FMNs at early stage following axotomy.

The aim of the study was to investigate the effect of exogenous glial cell line derived neurotrophic factor (GDNF) on spinal cord neurons after sciatic nerve axotomy. Upon silicone tubulization of transected sciatic nerve in the adult rat, either 0.9% saline or GDNF solution was injected into the silicone chamber. It was observed by Nissl and enzyme histochemistry staining that exogenous GDNF decreased lesion induced motor neuron death in lateral nucleus of spinal anterior horn and the changes in activity of cholinesterase and acid phosphatase in spinal cord and sensory ganglions. These results suggest that exogenous GDNF is capable of protecting motor neurons from death induced by peripheral nerve injury.