Pentylenetetrazole-Induced Seizures in Wistar Male Albino Rats with Reference to Glutamate Metabolism.

Journal of epilepsy research Pub Date : 2024-06-30 eCollection Date: 2024-06-01 DOI:10.14581/jer.24004
Sivaprasad Kanchi, Gurusekhar Meesala
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Abstract

Background and purpose: Epilepsy is a common and heterogenous neurological disorder characterized by recurrent spontaneous seizures. Animal models like rats play a crucial role in finding of mechanism of epilepsy in different brain regions. i.e., cerebral cortex, cerebellum, hippocampus, and pons medulla. Glutamate is an important excitatory neurotransmitter in the central nervous system and also glutamate plays a vital role in neuronal development and memory. The process of neuronal death evolved by glutamate receptor activation, has been hypothesized in both acute and chronic degenerative disorders including epilepsy. Considering the multifactorial neurochemical and neurophysiological malfunctions consequent to epileptic seizures, a few antiepileptic drugs are designed, to mitigate the debilitating aspects of epilepsy.

Methods: Rat model, pentylenetetrazole (PTZ), an anticonvulsant drug, was selected for the present study. Induction of epilepsy/convulsions was induced by an intraperitoneal injection of PTZ (60 mg/kg body weight) in saline. Biochemical assays performed through spectrophotometer.

Results: Glutamine and Glutamine synthetase levels were decreased in the epileptic rats brain regions i.e., hippocampus, cerebellum, cerebral cortex, and pons medulla; glutamate dehydrogenase and glutaminase levels were increased in all the regions of epilepsy induced rats. Highest values are recorded in hippocampus when compared to other brain regions.

Conclusion: PTZ suppresses the function of Glutamine and Glutamine synthetase activities in selected brain regions of rat and enhances the activities of the glutaminase and glutamate dehydrogenase when compared to control rats.

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戊烯四唑诱发 Wistar 雄性白化大鼠癫痫发作与谷氨酸代谢的关系
背景和目的:癫痫是一种常见的异质性神经系统疾病,以反复自发性癫痫发作为特征。大鼠等动物模型在发现不同脑区(即大脑皮层、小脑、海马和延髓)的癫痫机制方面发挥着至关重要的作用。谷氨酸是中枢神经系统中一种重要的兴奋性神经递质,谷氨酸还在神经元发育和记忆中发挥着重要作用。在包括癫痫在内的急性和慢性退行性疾病中,谷氨酸受体激活导致神经元死亡的过程被认为是一种假说。考虑到癫痫发作所导致的多因素神经化学和神经生理功能失调,我们设计了一些抗癫痫药物,以减轻癫痫所带来的衰弱:本研究选择了抗惊厥药物戊四唑(PTZ)作为大鼠模型。在生理盐水中腹腔注射 PTZ(60 毫克/千克体重)诱发癫痫/惊厥。通过分光光度计进行生化检测:结果:癫痫大鼠脑区(即海马、小脑、大脑皮层和脑髓)的谷氨酰胺和谷氨酰胺合成酶水平降低;诱导癫痫大鼠所有脑区的谷氨酸脱氢酶和谷氨酰胺酶水平升高。结论:PTZ 可抑制谷氨酸脱氢酶和谷氨酰胺酶的功能:结论:与对照组大鼠相比,PTZ 可抑制大鼠特定脑区谷氨酰胺和谷氨酰胺合成酶的活性,并增强谷氨酰胺酶和谷氨酸脱氢酶的活性。
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