Yao G L, Kiyama H
Department of Neuroanatomy, Osaka University Medical School, Japan.
Brain Res Mol Brain Res. 1995 Sep;32(2):308-12. doi: 10.1016/0169-328x(95)00091-6.
Application of dexamethasone was found to induce an enhanced expression level of mRNA encoding the growth associated protein (GAP-43) after peripheral nerve injury. Following hypoglossal nerve axotomy, a dexamethasone releasing pellet (1.5 mg released in 3 weeks) was placed near the transected nerve. GAP-43 mRNA was detected in the hypoglossal nucleus by non-radioactive in situ hybridization histochemistry using an alkaline phosphatase-labeled oligonucleotide probe. A significant elevation of GAP-43 mRNA level was observed 2 weeks after the transection in dexamethasone treated animals. This induction was not observed in the dorsal motor nucleus of vagus which expresses moderately high levels of GAP-43 mRNA even without nerve injury. Although dexamethasone did not alter the maximum level of GAP-43 mRNA in the hypoglossal nucleus after nerve injury, it prolonged the period in which the mRNA expression remained elevated. This may be due to post-transcriptional effect by the glucocorticoid. Dexamethasone treatment also caused a slight facilitation of reprojection. This may be due to the enhancement of GAP-43 mRNA level by the glucocorticoid.
研究发现，应用地塞米松可使周围神经损伤后编码生长相关蛋白（GAP - 43）的mRNA表达水平升高。舌下神经切断术后，将一个地塞米松缓释微丸（3周内释放1.5毫克）置于离断神经附近。使用碱性磷酸酶标记的寡核苷酸探针，通过非放射性原位杂交组织化学法在舌下神经核中检测到GAP - 43 mRNA。在切断术后2周，地塞米松处理的动物中观察到GAP - 43 mRNA水平显著升高。在迷走神经背运动核中未观察到这种诱导现象，即使在没有神经损伤的情况下，该核也表达中等高水平的GAP - 43 mRNA。尽管地塞米松并未改变神经损伤后舌下神经核中GAP - 43 mRNA的最高水平，但它延长了mRNA表达保持升高的时间。这可能是由于糖皮质激素的转录后效应。地塞米松治疗还略微促进了再投射。这可能是由于糖皮质激素提高了GAP - 43 mRNA水平。
