guanosine-diphosphate and Seizures

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.

Topics: Adenosine; Adenosine Diphosphate; Animals; Antigens, CD; Apyrase; Biomarkers; Brain; Convulsants; Disease Models, Animal; Female; Guanosine; Guanosine Diphosphate; Hydrolysis; Inosine; Nerve Degeneration; Nerve Growth Factors; Nerve Tissue Proteins; Pentylenetetrazole; Phosphopyruvate Hydratase; Purines; Rats; Rats, Wistar; S100 Calcium Binding Protein beta Subunit; S100 Proteins; Seizures; Time Factors; Up-Regulation