Stress, cytokines, and neural plasticity in depression Ja Wook Koo

ISBN: 9780549658900

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NOOKstudy eTextbook

162 pages


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Stress, cytokines, and neural plasticity in depression  by  Ja Wook Koo

Stress, cytokines, and neural plasticity in depression by Ja Wook Koo
| NOOKstudy eTextbook | PDF, EPUB, FB2, DjVu, AUDIO, mp3, ZIP | 162 pages | ISBN: 9780549658900 | 6.48 Mb

Depression is a very serious mental illness that affects nearly 20 percent of the US population and results in enormous personal suffering and socioeconomic burden. A major contributing factor to depression is uncontrollable stress, which canMoreDepression is a very serious mental illness that affects nearly 20 percent of the US population and results in enormous personal suffering and socioeconomic burden.

A major contributing factor to depression is uncontrollable stress, which can precipitate or exacerbate depression. Stress-induced reduction of hippocampal neurogenesis has been extensively investigated, based on the idea that the therapeutic effects of antidepressants involve a reversal of the stress-induced hippocampal impairment. However, the mechanisms underlying the anti-neurogenic and behavioral actions of stress to pathophysiology of depression remain ill defined. One possibility is interleukin (IL)-1beta, which is a pro-inflammatory cytokine that has been implicated as a mediator of stress and a causative factor in emotional disorders, including depression and anxiety.

In chapter 2, I demonstrate that IL-1beta underlies the anti-neurogenic effects of stress. Both acute and chronic stress suppressed hippocampal neurogenesis, of which the down-regulation was blocked by pre-administration of IL-1 receptor antagonist (Ra). The role of IL-1beta in the anti-neurogenic actions of acute and chronic stress was further confirmed in mice with a null mutation of the only effective IL-1beta receptor, IL-1RI.

In chapter 3, I show a role of IL-1beta in the anhedonic effects of chronic unpredictable stress (CUS). The pharmacological and genetic inactivation of IL-1RI blocked the anhedonic behavior resulting from CUS. Furthermore, I charaterized the role of IL-1beta in anxiety and fear models with IL-1RI null mice, which revealed that the IL-1beta/IL-1RI system may directly influence anxiety and fear memory formation. In chapter 4, I explore the mechanisms underlying the anti-proliferative actions of IL-1beta using cultured rat adult hippocampal progenitors.

I found that that IL-1beta and IL-1Ra act on cell proliferation via the IL-1R1 expressed on the neural progenitors. The anti-proliferative action of IL-1beta occurs through regulating the cell cycle, in particular, the expression of cyclin D1 and through activation of the nuclear factor-kappaB pathway in adult hippocampal progenitors. Taken together, my findings demonstrate that IL-1beta is a key mediator of stress on adult hippocampal neurogenesis and depression-related behaviors.



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