مشخصات مقاله | |
انتشار | مقاله سال 2018 |
تعداد صفحات مقاله انگلیسی | 10 صفحه |
هزینه | دانلود مقاله انگلیسی رایگان میباشد. |
منتشر شده در | نشریه الزویر |
نوع مقاله | ISI |
عنوان انگلیسی مقاله | Different behavioral and pathological changes between epilepsyassociated depression and primary depression models |
ترجمه عنوان مقاله | تغییرات رفتاری و پاتولوژیک بین افسردگی مرتبط با صرع و مدل افسردگی اولیه |
فرمت مقاله انگلیسی | |
رشته های مرتبط | پزشکی، روانشناسی |
گرایش های مرتبط | مغز و اعصاب، روانشناسی بالینی |
مجله | صرع و رفتار – Epilepsy & Behavior |
دانشگاه | Department of Neurology – Zhongshan Hospital – Fudan University – China |
کلمات کلیدی | صرع، افسردگی، رفتار، پروتئین اسیدی فیبریلاگر گلایال (GFAP)، میکروگلایا |
کلمات کلیدی انگلیسی | Epilepsy, Depression, Behavior, Glial fibrillary acidic protein (GFAP), Microglia |
شناسه دیجیتال – doi | https://doi.org/10.1016/j.yebeh.2017.12.038 |
کد محصول | E8183 |
وضعیت ترجمه مقاله | ترجمه آماده این مقاله موجود نمیباشد. میتوانید از طریق دکمه پایین سفارش دهید. |
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1. Introduction
Psychiatric disorders frequently occur in patients with epilepsy, in which depression is the most common comorbidity, with the prevalence of 20–50% [1–3]. However, the relationship between epilepsy and psychopathology is still poorly understood. Increased level of plasma corticosterone was found in the Chronic Unpredictable Mild Stress (CUMS)-induced depression model, a promising animal model for primary depression, and had a positive relationship with depressive behaviors [4–6]. Simultaneously, Mazarati 59 et al. [7,8] found that the chronic lithium chloride-pilocarpine rat epi- 60 lepsy model (Licl-pilocarpine model) which highly mimic temporal lobe epilepsy in humans [9] had elevated plasma corticosterone and depressive behaviors, suggesting that it could be served as a model for the comorbidity of epilepsy and depression. In addition, functional 64 disturbance of the hypothalamus–pituitary–adrenal (HPA) axis and high level circulating corticosterone was also found to contribute to 66 the incidence of depression in patients with epilepsy [10]. Although the high-level serum corticosterone and HPA axis dysfunc- tion might be the common pathophysiological mechanism both in 69 epilepsy-associated depression and primary depression, it could not ex- plain why epilepsy-associated depression is somewhat different from primary depression clinically because the clinical symptoms of depres-ion in patients with epilepsy are always atypical, complex, and easily unrecognized [11–13]. The symptoms of epilepsy-associated depression always have relative milder severity that does not meet DSM-IV criteria of major depressive disorder [11]. Suicidal idea, frustration intolerance, irritability, and motor agitation symptoms are unstable and can rapidly alternate with symptom-free periods, so Blumer et al. referred to it as interictal dysphoric disorder [12,13]. In this study, we aimed to compare the depressive-like behavioral and pathological changes between the chronic Licl-pilocarpine rat epilepsy model and CUMS rat depression model, trying to find some similarities and differences in epilepsyassociated depression and primary depression, helping to explain clinical correlations, and guiding diagnosis and treatment for patients with comorbidity of epilepsy and depression. |