Using optogenetics to translate the “inflammatory dialogue” between heart and brain in the context of stress

Cheng, Jinbo; Zhang, Jie; Lu, Caiyi; Wang, Li Ping

doi:10.1007/s12264-012-1246-2

Cited by 7 publications

(4 citation statements)

References 114 publications

(172 reference statements)

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“…Moreover, non-psychological disorders such as cardiovascular disease, diabetes, cancer, and rheumatoid arthritis can induce depression, which is also related to infl ammation with elevated levels of plasma IL-6, IL-17, and TNF-α [23][24][25] . In addition, the new technology of optogenetics can be applied to understand the infl ammatory process in psychiatric disorders and cardiovascular diseases, representing a potential dialogue between heart and brain [26] . All this evidence hints at a bidirectional of depressive patients and animal models of depression [3,4] .…”

Section: Sources Of Cytokines In the Brainmentioning

confidence: 99%

Inflammation: a mechanism of depression?

Han

2014

Neurosci. Bull.

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In recent decades, major depression has become more prevalent and research has shown that immune activation and cytokine production may be involved. This review is mainly focused on the contribution of infl ammation to depression. We fi rst briefl y introduce the infl ammatory biomarkers of depression, then discuss the sources of cytokines in the brain, and fi nally describe the neuroimmunological mechanisms underlying the association between infl ammation and depression.Keywords: depression; infl ammation; cytokines; hypothalamic-pituitary-adrenal axis; 5-HT; neuroplasticity ·Review· IntroductionThe prevalence of major depression has increased dramatically over the past few decades [1] , and women are nearly twice as likely as men to develop depressive disorder [2] . Depression is classified as a brain disorder, but its symptomatology includes some behaviors that also occur during chronic infl ammatory stress [3] . Research has shown that immune activation and the production of cytokines may be involved in depression [4] , so this relationship has received much attention. In fact, three causal pathways have been proposed: depression to inflammation, inflammation to depression, and a bidirectional relationship [5] . In this review, we focus on the impact of inflammation on depression and the underlying mechanisms. Cytokines are small cell-signaling proteins that mediate and regulate immune responses and inflammation, and can be divided into two categories:the pro-inflammatory cytokines interleukin (IL)-1 β, IL-6, IL-8, and tumor necrosis factor (TNF)-α, and the anti-inflammatory cytokines IL-1Rα, IL-4, IL-10, and transforming growth factor (TGF)-β1. Generally, t he proinfl ammatory cytokines promote systemic infl ammation and are essential for the initiation of an infl ammatory response to disease [6] , while the anti-inflammatory cytokines antagonize these actions to reduce inflammation and promote healing [6,7] . Moreover, some cytokines play dual roles [8] . In the central nervous system (CNS), the cellular source, function, and mechanisms of action of cytokines differ from those in the periphery. In the following, we briefl y introduce the current research on infl ammatory biomarkers of depression. Infl ammatory Biomarkers of DepressionSo far, there are neither universally accepted or defi nitive biomarkers of depression [9] , nor effective methods to assess the severity, endophenotypes, or response to treatment [10] .However, sufficient evidence has suggested changes in the circulating levels of cytokines in depressed patients, which can be reversed by antidepressant treatments [11,12] .So, many studies have aimed to clarify the neurobiological changes in depression and to establish inflammatory biomarkers. The peripheral levels of IL-6, TNF-α, and IL-1β are increased in patients with depression [13][14][15][16][17] , and antidepressant treatments reverse this effect [18][19][20] . These consistent results demonstrate that IL-6, TNF-α, and IL-1β are putative biomarkers for depression. However, due to the he...

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Section: Sources Of Cytokines In the Brainmentioning

confidence: 99%

Inflammation: a mechanism of depression?

Han

2014

Neurosci. Bull.

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“… 9 Yet, a third model posits a shared liability—i.e., the same factors that increase risk for one disorder may increase risk for the other. 10 Multiple twin or family investigations support this shared liability, at least for cardiovascular disease. 11 , 12 , 13 In reality, it is likely that all three mechanisms play a role in co-occurrence of some disorders, but confirming the presence of at least one mechanism would represent a key first step in understanding these relationships.…”

Section: Introductionmentioning

confidence: 99%

Polygenic loading for major depression is associated with specific medical comorbidity

et al. 2017

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Major depressive disorder frequently co-occurs with medical disorders, raising the possibility of shared genetic liability. Recent identification of 15 novel genetic loci associated with depression allows direct investigation of this question. In cohorts of individuals participating in biobanks at two academic medical centers, we calculated polygenic loading for risk loci reported to be associated with depression. We then examined the association between such loading and 50 groups of clinical diagnoses, or topics, drawn from these patients' electronic health records, determined using a novel application of latent Dirichilet allocation. Three topics showed experiment-wide association with the depression liability score; these included diagnostic groups representing greater prevalence of mood and anxiety disorders, greater prevalence of cardiac ischemia, and a decreased prevalence of heart failure. The latter two associations persisted even among individuals with no mood disorder diagnosis. This application of a novel method for grouping related diagnoses in biobanks indicate shared genetic risk for depression and cardiac disease, with a pattern suggesting greater ischemic risk and diminished heart failure risk.

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“…In parallel to studies aimed to untangle central neuronal circuitries impacting on heart activity in physiology, optogenetics was also applied to complex neuro-cardiac pathologies, including e.g., the study of the bidirectional link between psychiatric disorders and heart diseases (Cheng et al, 2012 ).…”

Section: Can Optogenetics Uncoil the Intertwined Brain-to-heart Connections?mentioning

confidence: 99%

Neurohumoral Cardiac Regulation: Optogenetics Gets Into the Groove

et al. 2021

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The cardiac autonomic nervous system (ANS) is the main modulator of heart function, adapting contraction force, and rate to the continuous variations of intrinsic and extrinsic environmental conditions. While the parasympathetic branch dominates during rest-and-digest sympathetic neuron (SN) activation ensures the rapid, efficient, and repeatable increase of heart performance, e.g., during the “fight-or-flight response.” Although the key role of the nervous system in cardiac homeostasis was evident to the eyes of physiologists and cardiologists, the degree of cardiac innervation, and the complexity of its circuits has remained underestimated for too long. In addition, the mechanisms allowing elevated efficiency and precision of neurogenic control of heart function have somehow lingered in the dark. This can be ascribed to the absence of methods adequate to study complex cardiac electric circuits in the unceasingly moving heart. An increasing number of studies adds to the scenario the evidence of an intracardiac neuron system, which, together with the autonomic components, define a little brain inside the heart, in fervent dialogue with the central nervous system (CNS). The advent of optogenetics, allowing control the activity of excitable cells with cell specificity, spatial selectivity, and temporal resolution, has allowed to shed light on basic neuro-cardiology. This review describes how optogenetics, which has extensively been used to interrogate the circuits of the CNS, has been applied to untangle the knots of heart innervation, unveiling the cellular mechanisms of neurogenic control of heart function, in physiology and pathology, as well as those participating to brain–heart communication, back and forth. We discuss existing literature, providing a comprehensive view of the advancement in the understanding of the mechanisms of neurogenic heart control. In addition, we weigh the limits and potential of optogenetics in basic and applied research in neuro-cardiology.

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Using optogenetics to translate the “inflammatory dialogue” between heart and brain in the context of stress

Cited by 7 publications

References 114 publications

Inflammation: a mechanism of depression?

Inflammation: a mechanism of depression?

Polygenic loading for major depression is associated with specific medical comorbidity

Neurohumoral Cardiac Regulation: Optogenetics Gets Into the Groove

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