Department of Human Physiology, College of Health Sciences, University of Kwazulu-Natal, South Africa.
Department of Human Physiology, College of Health Sciences, University of Kwazulu-Natal, South Africa.
Life Sci. 2020 Jul 15;253:117692. doi: 10.1016/j.lfs.2020.117692. Epub 2020 May 3.
Depression is the most significant cause of suicide among neuropsychiatric illnesses. Major depression further affects the quality of life in an individual with epilepsy. The treatment of depression in an epileptic patient could be very challenging because of drug selection or the fact that some antiepileptic drugs are known to cause depression. It has been shown that in addition to the known involvement of the serotonergic pathway in depression, the glutamatergic system is also involved in the evolution of the disease, but this knowledge is limited. This study assessed if induction of epilepsy in rats will cause depressive-like behavior, alters the concentrations of metabotropic receptor 5 (mGluR5), glutamate transport protein (GLAST), glutamate synthase (GS) and brain derived neurotrophic factor (BDNF).
Epilepsy was induced in rats by injecting Pentylenetetrazole at 35 mg/kg every other day. At kindle, rats were subjected to sucrose preference test (SPT) and forced swim test (FST) and decapitated 4 h later. Hippocampal tissue was collected and the BDNF concentration was measured with ELISA; mGluR5 and GS protein expression was measured using western blot while amygdala tissue was used for GLAST expression with flow cytometry.
Our results showed that epilepsy leads to depressive-like behavior in rats and alters the glutamatergic system.
Therefore, we conclude that targeting the glutamate pathway may be a good strategy to alleviate depressive-like behavior associated with epilepsy.
抑郁症是神经精神疾病中导致自杀的最主要原因。重度抑郁症进一步影响癫痫患者的生活质量。由于药物选择或某些抗癫痫药物已知会引起抑郁，因此癫痫患者的抑郁治疗可能极具挑战性。已经表明，除了已知的 5-羟色胺能途径参与抑郁症外，谷氨酸能系统也参与疾病的发展，但这方面的知识有限。本研究评估了在大鼠中诱导癫痫是否会引起类似抑郁的行为，改变代谢型谷氨酸受体 5 (mGluR5)、谷氨酸转运蛋白 (GLAST)、谷氨酸合酶 (GS) 和脑源性神经营养因子 (BDNF) 的浓度。
通过每隔一天向大鼠注射 35mg/kg 的戊四氮来诱导癫痫。在癫痫发作时，大鼠接受蔗糖偏好测试（SPT）和强迫游泳测试（FST），4 小时后断头。收集海马组织，用 ELISA 测量 BDNF 浓度；使用 Western blot 测量 mGluR5 和 GS 蛋白表达，使用流式细胞术测量杏仁核组织的 GLAST 表达。
我们的结果表明，癫痫导致大鼠出现类似抑郁的行为，并改变了谷氨酸能系统。
因此，我们得出结论，靶向谷氨酸途径可能是缓解与癫痫相关的类似抑郁行为的一种好策略。
