Testosterone Treatment Attenuates the Effects of Facial Nerve Transection on Glial Fibrillary Acidic Protein (GFAP) Levels in the Hamster Facial Motor Nucleus

Testosterone propionate (TP) administration coincident with facial nerve injury accelerates the recovery rate from facial muscle paralysis in the hamster. One mechanism by which TP could augment peripheral nerve regeneration is through glial fibrillary acidic protein the facial motor nucleus. In a previous study, axotomy alone induces increases in GFAP mRNA, with TP significantly attenuating the axotomy-induced increases in GFAP mRNA. In the present study, immunoblotting techniques were used to extend our previous GFAP mRNA studies to the protein level. Castrated male hamsters were subjected to a right facial nerve transection, with half of the animals receiving subcutaneous implants of 100% crystalline TP. The left facial motor nucleus of each animal served as an internal control. Postoperative survival times include Days 4, 7, and 14. In non–TP-treated animals, facial nerve transections alone increased GFAP levels at all time points, relative to internal controls. As previously observed at the mRNA level, TP treatment attenuated but did not eliminate the axotomy-induced increase in GFAP levels at all time points tested. These results suggest that the regulatory actions of gonadal steroids on GFAP expression manifested in parallel at the mRNA/protein levels.     

Self-remitting Elevation of Adenosine Deaminase Levels in the Cerebrospinal Fluid with Autoimmune Glial Fibrillary Acidic Protein Astrocytopathy: A Case Report and Review of the Literature

A 29-year-old man presented with a high-grade fever, headache, and urinary retention, in addition to meningeal irritation and myoclonus in his upper extremities. A cerebrospinal fluid (CSF) examination showed pleocytosis and high adenosine deaminase (ADA) levels with no evidence of bacterial infection, including Mycobacterium tuberculosis. T2-weighted brain magnetic resonance imaging showed transient hyper-intensity lesions at the splenium of the corpus callosum (SCC), bilateral putamen, and pons during the course of the disease. The CSF was positive for anti-glial fibrillary acidic protein (GFAP) antibodies. He was diagnosed with autoimmune GFAP astrocytopathy. The present case shows that the combination of an elevated ADA level in the CSF and reversible T2-weighted hyper-intensity on the SCC supports the diagnosis of autoimmune GFAP encephalopathy.     

骨保护素和骨唾液蛋白在风湿钙化二尖瓣的表达及意义

目的观察骨保护素和骨唾液蛋白在风湿性心脏病(风心病)二尖瓣的表达。方法将手术切除的42枚二尖瓣分为风心病组24枚和非风心病组18枚,采用免疫组化染色观察骨保护素和骨唾液蛋白在两组的表达。结果风心病组的骨保护素(P<0.001)和骨唾液蛋白(P<0.001)均较非风心病组表达增高。结论在风心病瓣膜中,骨保护素和骨唾液蛋白均呈现高表达,表明风心病瓣膜钙化并非简单的钙盐沉积,很可能是成骨样骨形成。     

瑞香素对脑缺血再灌注大鼠模型胶质纤维酸性蛋白表达的影响

目的探讨瑞香素对大鼠前脑缺血再灌注后海马和皮层胶质纤维酸性蛋白（glial fibrillary acidic protein,GFAP）表达的影响.方法反复夹闭大鼠双侧颈总动脉模仿人类脑缺血制备前脑缺血再灌注模型,术后给予瑞香素灌胃治疗,免疫组化法检测脑缺血再灌注后2、4、6 w海马和皮层GFAP的表达.结果瑞香素治疗后,海马和皮层GFAP的表达在2 w时较假手术组和缺血再灌注组高,然后开始下降,4 w时低于缺血再灌注组但高于假手术组,6 w时已低于假手术组;瑞香素治疗组中,随着时间延长,GFAP的表达进行性下降,差异显著.结论大鼠前脑缺血再灌注后应用瑞香素治疗对海马和皮层GFAP表达的影响呈动态变化过程,表现为早期促进表达,后期抑制表达,这种调节作用可能与脑缺血性损伤后神经保护有关.     

Ethanol Decreases Glial Derived Neurotrophic Factor (GDNF) Protein Release but Not mRNA Expression and Increases GDNF-Stimulated Shc Phosphorylation in the Developing Cerebellum

BACKGROUND: Ethanol exposure during development leads to substantial neuronal loss in multiple regions of the brain. Although differentiating Purkinje cells of the cerebellum are particularly vulnerable to ethanol exposure, the mechanisms underlying ethanol-induced Purkinje cell loss have not been well defined. Our previous research indicated that exogenous Glial-Derived Neurotrophic Factor (GDNF) attenuated ethanol-induced Purkinje cell loss in cerebellar explant cultures, which suggests that ethanol, in turn, may decrease endogenous trophic factor-mediated survival mechanisms. METHODS: The present experiments used an explant culture model of the developing rat cerebellum to test the hypothesis that ethanol decreases endogenous trophic support by limiting the availability of trophic factors, such as GDNF, or by altering the activation of key adapter proteins such as Shc (Src homology domain carboxy-terminal) that couple GDNF binding to multiple intracellular signaling pathways. GDNF mRNA and protein levels were measured by reverse northern blot analysis and sandwich enzyme-linked immunosorbent assay respectively, whereas Shc phosphorylation was measured by immunoprecipitation/western immunoblot analysis. RESULTS: The developing cerebellum expresses both GDNF mRNA and protein in vitro. Ethanol exposure (68, 103, or 137 mM) had no effect on cerebellar levels of GDNF mRNA. However, ethanol (68 and 137 mM) decreased levels of GDNF protein released into culture medium. In addition, ethanol itself had no effect on She phosphorylation. However, in the presence of the highest dose of ethanol (137 mM) GDNF did stimulate Shc phosphorylation. CONCLUSIONS: Together, these results suggest that ethanol decreases GDNF-mediated trophic support of Purkinje cells in the developing cerebellum. However, GDNF in turn activates intracellular signaling pathways throughout the developing cerebellum as part of its Purkinje cell-selective neuroprotective response to ethanol exposure.     

针刺筋会穴阳陵泉对帕金森模型小鼠黑质TH和GFAP表达的影响

目的 观察比较1-甲基-4-苯基-1,2,3,6四氢吡啶(MPTP) 诱导的帕金森小鼠模型及其接受针刺治疗后黑质酪氨酸羟化酶(TH)和星形胶质细胞的胶质原纤维性蛋白(GFAP)的表达变化.方法 以腹腔注射(30 mg/kg) MPTP诱导7 d形成帕金森小鼠模型,针刺双侧筋会穴"阳陵泉"及"舞蹈震颤区",每日1次共治疗21 d.针刺结束后,采用免疫荧光组化检测小鼠脑黑质TH的和GFAP的表达变化.结果 在7 d造模后,模型组和针刺组TH阳性细胞显著丢失;治疗结束后,与模型组比较,针刺组TH 阳性细胞数量增加,正常组和针刺组GFAP的阳性细胞数量减少.结论 MPTP可促进帕金森模型小鼠表达;针刺筋会穴阳陵泉可对MPTP 诱导小鼠黑质多巴胺能神经有保护作用,能明显地减弱MPTP伤害性刺激引起的行为反应.