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BACKGROUND:Gamma-aminobutyric acid transporter plays an important role in gamma-aminobutyric acid metabolism,and is highly associated with epilepsy seizures. Pathologically,astrocytes release active substances that alter neuronal excitability,and it has been demonstrated that astrocytes play a role in epileptic seizures. OBJECTIVE:To observe changes in gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression in the hippocampus and cortex of the temporal lobe in rats with pentylenetetrazol-induced chronic epilepsy. DESIGN,TIME AND SETTING:Randomized,controlled,animal experiment was performed at the Department of Neurobiology,Third Military University of Chinese PLA between January 2006 and December 2007. MATERIALS:Pentylenetetrazol was purchased from Sigma,USA;rabbit anti-rat gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein were from Chemicon,USA. METHODS:A total of 40 Sprague Dawley rats were divided into model and control groups.Rat models of chronic epilepsy were created by pentylenetetrazol kindling,and were subdivided into 3-,7-,and 14-day kindling subgroups. MAIN OUTCOME MEASURES:Gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression,as well as the number of positive cells in the hippocampus and cortex of temporal lobe of rats,were determined by immunohistochemistry and Western blot analyses. RESULTS:Compared with the control group,the number of gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein -positive cells in the hippocampus and cortex of rats with pentylenetetrazol-induced epilepsy significantly increased,gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression increased after 3 days of kindling,reached a peak on day 7,and remained at elevated levels at day 14(P<0.05). CONCLUSION:Astrocytic activation and gamma-aminobutyric acid transporter 1 overexpression may contribute to pentylenetetrazol-induced epilepsy.
BACKGROUND: Gamma-aminobutyric acid transporter plays an important role in gamma-aminobutyric acid metabolism, and is highly associated with epilepsy seizures. Pathologically, astrocytes release active substances that alter neuronal excitability, and it has been demonstrated that astrocytes play a role in epileptic seizures . OBJECTIVE: To observe changes in gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression in the hippocampus and cortex of the temporal lobe in rats with pentylenetetrazol-induced chronic epilepsy. DESIGN, TIME AND SETTING: Randomized, controlled, animal experiment was performed at the Department of Neurobiology, Third Military University of Chinese PLA between January 2006 and December 2007. MATERIALS: Pentylenetetrazol was purchased from Sigma, USA; rabbit anti-rat gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein were from Chemicon, USA METHODS: A total of 40 Sprague Dawley rats were divided into model and control groups. Rat models of chronic epilepsy were created by pentylenetetrazol kindling, and were subdivided into 3-, 7-, and 14-day kindling subgroups. MAIN OUTCOME MEASURES: Gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression, as well as the number of positive cells in the hippocampus and cortex of temporal lobe of rats, were determined by immunohistochemistry and Western blot analyzes. RESULTS: Compared with the control group, the number of gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein-positive cells in the hippocampus and cortex of rats with pentylenetetrazol-induced epilepsy significantly increased, gamma-aminobutyric acid transporter 1 and glial fibrillary acidic protein expression increased after 3 days of kindling, reached a peak on day 7, and remained at elevated levels at day 14 (P <0.05 CONCLUSION: Astrocytic activation and gamma-aminobutyric acid transporter 1 overexpression may contribute to pentylenetetrazol-induced epilepsy.