Stroke, stress, and depression–evidence from a brain ischemia mouse model
Başlık çevirisi mevcut değil.
- Tez No: 401348
- Danışmanlar: PROF. DR. MATTHIAS ENDRES
- Tez Türü: Doktora
- Konular: Nöroloji, Neurology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2014
- Dil: İngilizce
- Üniversite: Charité–Universitätsmedizin Berlin
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 51
Özet
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Özet (Çeviri)
Emerging evidence in the last decade points out an association between stress, depression and stroke. Clinical studies report that a considerable portion of stroke survivors develop depression after stroke. Also, an increasing number of clinical case-control studies indicate an association between stress levels and ischemic stroke. Experimental studies focusing on the bi-directional interaction between stroke and stress as well as depression are crucial to better understand the pathophysiology of stroke and depression. This PhD work focuses on three separate projects that investigate the nature and mechanisms of this relationship. In study 1 the effects of 30 minutes left and right middle cerebral artery occlusion (MCAo) on mouse“anxiety”-like and“depression”-like behavior were evaluated. Left MCAo but not right MCAo led to chronic depression and anxiety-like behavior; citalopram treatment was shown to reverse these effects. 30 min MCAo caused significant and chronic reduction of striatal dopamine (DA) levels. Striatal DA loss was normalized to a large degree by citalopram treatment. Further histological analysis revealed a significant loss of dopaminergic neurons in ipsilateral ventral tegmental area (VTA) and Substantio Nigra (SN), as assessed by Tyrosine Hydroxylase (TH) immunostaining and NeuN-immunostaining. Cell loss in SN and VTA, and effects of MCAo were also significantly attenuated by citalopram treatment. Our study indicate that it is possible to model Post stroke depression in mouse models and provide interesting findings regarding the possible mechanisms that result in the observed changes, such as sustained depletion of dopamine. Study 2 and 3 investigate the effects of chronic stress on stroke outcome, endothelial function and oxidative stress load. Over the course of four weeks animals were exposed to a chronic stress procedure. Animals of the treatment group were given the I(f)-channel inhibitor ivabradine or glucocorticoid antagonist mifepristone. In both studies stress exposure increased adrenal gland weight, overall corticosterone levels and increased the lesion size after MCAo. Heart rate was both acutely and chronically elevated in the stressed mice. Both studies confirmed that chronic stress exposure impairs endothelium function and down regulates eNOS mRNA levels in the brain and aorta along with increasing the markers of oxidative stress. Both Ivabradine and mifepristone treatment reduced lesion size, normalized endothelial dysfunction and reduced oxidative burden. Both studies indicate that a significant reduction in endothelial function along with markedly increased oxidative stress may be a possible pathway by which stress can facilitate stroke
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