تغییرات رفتاری و پاتولوژیک بین افسردگی مرتبط با صرع و مدل افسردگی اولیه / Different behavioral and pathological changes between epilepsyassociated depression and primary depression models

تغییرات رفتاری و پاتولوژیک بین افسردگی مرتبط با صرع و مدل افسردگی اولیه Different behavioral and pathological changes between epilepsyassociated depression and primary depression models

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • ناشر : Elsevier
  • چاپ و سال / کشور: 2018

توضیحات

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
شناسه دیجیتال – doi https://doi.org/10.1016/j.yebeh.2017.12.038
منتشر شده در نشریه الزویر
کلمات کلیدی انگلیسی Epilepsy, Depression, Behavior, Glial fibrillary acidic protein (GFAP), Microglia

Description

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.
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