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神经节苷脂GM1治疗对大鼠纹状体葡萄糖代谢、血流及蛋白质磷酸化的影响。

Effects of ganglioside GM1 treatment on striatal glucose metabolism, blood flow, and protein phosphorylation of the rat.

作者信息

Agnati L F, Fuxe K, Benfenati F, Zoli M, Owman C, Diemer N H, Kåhrström J, Toffano G, Cimino M

出版信息

Acta Physiol Scand. 1985 Sep;125(1):43-53. doi: 10.1111/j.1748-1716.1985.tb07691.x.

Abstract

Effects of ganglioside GM1 administration have been studied in unilaterally partially hemitransected rats on striatal energy metabolism, using the radioactive deoxyglucose (DG) technique, on striatal blood flow, using radiolabelled iodoantipyrine (IAP) as tracer, and on cyclic AMP (cAMP) and Ca2+ induced protein phosphorylation in striatal membranes (P2 fraction). Ganglioside GM1 treatment counteracted the imbalance in striatal energy metabolism, in striatal blood flow, as well as in protein phosphorylation found between the striata of the lesioned and unlesioned side, possibly due to excitatory effects on the lesioned side and inhibitory effects on the unlesioned side. In intact animals, GM1 treatment produced a reduction in cAMP and Ca2+ induced striatal protein phosphorylation. Facilitatory actions of the ganglioside GM1 dominate following a lesion, probably due to its possible function as a modulator of receptors for neuronotrophic factors, leading to restoration of metabolic rate and of cAMP and Ca2+ induced protein phosphorylation in the striatum of the lesioned side. The results emphasize that ganglioside GM1 treatment can restore the metabolism of a partially innervated striatum towards normal, as evaluated both at the level of the entire striatal structure by means of the DG and IAP techniques and at the molecular level by means of studies on the cAMP and Ca2+ induced protein phosphorylation.

摘要

采用放射性脱氧葡萄糖(DG)技术,研究了神经节苷脂GM1给药对单侧部分半横断大鼠纹状体能量代谢的影响;采用放射性碘代安替比林(IAP)作为示踪剂,研究了其对纹状体血流量的影响;并研究了其对纹状体膜(P2部分)中环磷酸腺苷(cAMP)和Ca2+诱导的蛋白质磷酸化的影响。神经节苷脂GM1治疗抵消了损伤侧和未损伤侧纹状体之间在能量代谢、血流量以及蛋白质磷酸化方面的不平衡,这可能是由于其对损伤侧的兴奋作用和对未损伤侧的抑制作用。在完整动物中,GM1治疗使cAMP和Ca2+诱导的纹状体蛋白质磷酸化减少。损伤后神经节苷脂GM1的促进作用占主导,这可能是由于其作为神经营养因子受体调节剂的可能功能,导致损伤侧纹状体的代谢率以及cAMP和Ca2+诱导的蛋白质磷酸化恢复。结果强调,通过DG和IAP技术在整个纹状体结构水平以及通过对cAMP和Ca2+诱导的蛋白质磷酸化的研究在分子水平评估,神经节苷脂GM1治疗可使部分神经支配的纹状体代谢恢复正常。

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