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戊四氮诱发癫痫后大鼠脑脊液中的生化脑标志物和嘌呤能参数

Biochemical brain markers and purinergic parameters in rat CSF after seizure induced by pentylenetetrazol.

作者信息

Oses Jean Pierre, Leke Renata, Portela Luis Valmor, Lara Diogo R, Schmidt André P, Casali Emerson André, Wofchuk Susana, Souza Diogo O, Sarkis João José Freitas

机构信息

Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos, 2600 anexo, 90035-003, Porto Alegre, RS, Brazil.

出版信息

Brain Res Bull. 2004 Sep 30;64(3):237-42. doi: 10.1016/j.brainresbull.2004.07.006.

DOI:10.1016/j.brainresbull.2004.07.006
PMID:15464860
Abstract

Cellular and molecular mechanisms involved in the generation of seizures and the magnitude of neural cells injury are not fully understood. We evaluated astrocyte and/or neuronal injury in rats in the pentylenetetrazol model of acute seizures by measuring S100B and NSE levels in cerebrospinal fluid. Additionally, we determined ADP and GDP hydrolysis by soluble nucleoside triphosphate diphosphohydrolase in the cerebrospinal fluid, and the concentration of nucleosides adenosine, inosine and guanosine as putative markers of brain injury. After pentylenetetrazol-induced seizures: (i) S100B values increased from 10 to 30 min, returning to control levels at 24 h; NSE levels presented a biphasic increase: an increase at 10 to 30 min returning to control levels, and again at 240 min followed by a decline at 24 h; (ii) nucleotidase activities increased from 10 min, returning to control levels at 240 min; (iii) guanosine and inosine levels increased exclusively after 30 min. In summary, this study showed biochemical changes in the cerebrospinal fluid occurring after seizures induced by pentylenetetrazol. Such events may have a modulating effect upon seizure expression, particularly nucleoside triphosphate diphosphohydrolase activities and nucleoside concentrations, but are nevertheless followed by neural death as evidenced by the increase in NSE and S100B levels.

摘要

癫痫发作的产生以及神经细胞损伤程度所涉及的细胞和分子机制尚未完全明确。我们通过测量脑脊液中S100B和NSE的水平,评估了戊四氮急性癫痫模型大鼠中的星形胶质细胞和/或神经元损伤。此外,我们测定了脑脊液中可溶性核苷三磷酸二磷酸水解酶的ADP和GDP水解情况,以及作为脑损伤假定标志物的腺苷、肌苷和鸟苷核苷的浓度。在戊四氮诱发癫痫发作后:(i)S100B值在10至30分钟时升高,在24小时时恢复至对照水平;NSE水平呈双相升高:在10至30分钟时升高并恢复至对照水平,在240分钟时再次升高,随后在24小时时下降;(ii)核苷酸酶活性从10分钟起升高,在240分钟时恢复至对照水平;(iii)鸟苷和肌苷水平仅在30分钟后升高。总之,本研究显示了戊四氮诱发癫痫发作后脑脊液中的生化变化。这些事件可能对癫痫发作表现具有调节作用,特别是核苷三磷酸二磷酸水解酶活性和核苷浓度,但如NSE和S100B水平升高所证明的,随后会出现神经死亡。

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