Literature DB >> 22833041

Using optogenetics to translate the "inflammatory dialogue" between heart and brain in the context of stress.

Jinbo Cheng1, Jie Zhang, Caiyi Lu, Liping Wang.   

Abstract

Inflammatory processes are an integral part of the stress response and are likely to result from a programmed adaptation that is vital to the organism's survival and well-being. The whole inflammatory response is mediated by largely overlapping circuits in the limbic forebrain, hypothalamus and brainstem, but is also under the control of the neuroendocrine and autonomic nervous systems. Genetically predisposed individuals who fail to tune the respective contributions of the two systems in accordance with stressor modality and intensity after adverse experiences can be at risk for stress-related psychiatric disorders and cardiovascular diseases. Altered glucocorticoid (GC) homeostasis due to GC resistance leads to the failure of neural and negative feedback regulation of the hypothalamic-pituitary-adrenal axis during chronic inflammation, and this might be the mechanism underlying the ensuing brain and heart diseases and the high prevalence of co-morbidity between the two systems. By the combined use of light and genetically-encoded light-sensitive proteins, optogenetics allows cell-type-specific, fast (millisecond-scale) control of precisely defined events in biological systems. This method is an important breakthrough to explore the causality between neural activity patterns and behavioral profiles relevant to anxiety, depression, autism and schizophrenia. Optogenetics also helps to understand the "inflammatory dialogue", the inflammatory processes in psychiatric disorders and cardiovascular diseases, shared by heart and brain in the context of stress.

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Year:  2012        PMID: 22833041      PMCID: PMC5560261          DOI: 10.1007/s12264-012-1246-2

Source DB:  PubMed          Journal:  Neurosci Bull        ISSN: 1995-8218            Impact factor:   5.203


  111 in total

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Review 4.  Physiology of microglia.

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Review 5.  Effects of stress on the immune system.

Authors:  D N Khansari; A J Murgo; R E Faith
Journal:  Immunol Today       Date:  1990-05

6.  Neuroendocrine and cytokine profile of chronic mild stress-induced anhedonia.

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7.  Brain interleukin-1 mediates chronic stress-induced depression in mice via adrenocortical activation and hippocampal neurogenesis suppression.

Authors:  I Goshen; T Kreisel; O Ben-Menachem-Zidon; T Licht; J Weidenfeld; T Ben-Hur; R Yirmiya
Journal:  Mol Psychiatry       Date:  2007-08-14       Impact factor: 15.992

Review 8.  Inflammation and cortisol response in coronary artery disease.

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Journal:  Ann Med       Date:  2009       Impact factor: 4.709

9.  Involvement of tumor necrosis factor-alpha in angiotensin II-mediated effects on salt appetite, hypertension, and cardiac hypertrophy.

Authors:  Srinivas Sriramula; Masudul Haque; Dewan S A Majid; Joseph Francis
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10.  Optogenetics.

Authors:  Karl Deisseroth
Journal:  Nat Methods       Date:  2010-12-20       Impact factor: 28.547

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  3 in total

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Review 2.  Inflammation: a mechanism of depression?

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Journal:  Neurosci Bull       Date:  2014-05-16       Impact factor: 5.203

3.  Polygenic loading for major depression is associated with specific medical comorbidity.

Authors:  T H McCoy; V M Castro; L Snapper; K Hart; J L Januzzi; J C Huffman; R H Perlis
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  3 in total

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