Association between increased inflammatory cytokine expression in the lateral habenular nucleus and depressive-like behavior induced by unpredictable chronic stress in rats

Wang, Yachun; Qu, Peng; Sun, Yu; Li, Ziang; Liu, Lei; Yang, Limin

doi:10.1016/j.expneurol.2021.113964

Cited by 15 publications

(21 citation statements)

References 41 publications

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“…Chronic unpredictable stress (CUS) increases the nuclear factor-κB (NF-kB) signaling pathway expression in the LHb, and injection of TNF-α into the LHb leads to depressive-like behavior in rats, which is conversely reduced by anti-inflammatory aspirin or NF-kB inhibitors [ 79 ]. Destruction of the LHb reduces inflammatory responses in the hippocampus and ameliorates hippocampal degeneration by reducing the expression of the PI3K/mTOR signaling pathway and apoptosis-related proteins, including phosphorylated p53, Bax, Bcl-2, and cleaved-caspase3, demonstrating the role of inflammatory responses of the LHb in depression [ 79 ].…”

Section: Inflammatory Changes In the Specific Brain Regions Of Associ...mentioning

confidence: 99%

Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression

et al. 2023

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Mood disorders are associated with elevated inflammation, and the reduction of symptoms after multiple treatments is often accompanied by pro-inflammation restoration. A variety of neuromodulation techniques that regulate regional brain activities have been used to treat refractory mood disorders. However, their efficacy varies from person to person and lack reliable indicator. This review summarizes clinical and animal studies on inflammation in neural circuits related to anxiety and depression and the evidence that neuromodulation therapies regulate neuroinflammation in the treatment of neurological diseases. Neuromodulation therapies, including transcranial magnetic stimulation (TMS), transcranial electrical stimulation (TES), electroconvulsive therapy (ECT), photobiomodulation (PBM), transcranial ultrasound stimulation (TUS), deep brain stimulation (DBS), and vagus nerve stimulation (VNS), all have been reported to attenuate neuroinflammation and reduce the release of pro-inflammatory factors, which may be one of the reasons for mood improvement. This review provides a better understanding of the effective mechanism of neuromodulation therapies and indicates that inflammatory biomarkers may serve as a reference for the assessment of pathological conditions and treatment options in anxiety and depression.

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Section: Inflammatory Changes In the Specific Brain Regions Of Associ...mentioning

confidence: 99%

Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression

et al. 2023

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“…These researchers observed an increase of inflammatory cytokines in the CNS, especially in the LHb; conversely, local administration of tumor necrosis factor- alpha in the LHb, can induce depressive-like behaviour in control rats. Lastly, they showed that lesioning LHb prevented the impairment of hippocampal neurogenesis and a reduction of the hippocampal function in UCS exposed rats [151].…”

Section: Role Of the Lhb In Depression Associated Inflammationmentioning

confidence: 97%

“…A recent interesting study investigated the role of the LHb in depression-associated inflammation by using the Unpredictable Chronic Stress (UCS) animal model of depression [151]. These researchers observed an increase of inflammatory cytokines in the CNS, especially in the LHb; conversely, local administration of tumor necrosis factor- alpha in the LHb, can induce depressive-like behaviour in control rats.…”

Section: Role Of the Lhb In Depression Associated Inflammationmentioning

confidence: 99%

BDNF Alterations in Brain Areas and the Neurocircuitry Involved in the Antidepressant Effects of Ketamine in Animal Models, Suggest the Existence of a Primary Circuit of Depression

Carboni¹,

Carta²

2022

J. Integr. Neurosci.

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Major depressive disorder is one of the primary causes of disability and disease worldwide. The therapy of depression is prevalently based on monoamine reuptake blockers; consequently, investigations aimed to clarify the aetiology of depression have mostly looked at brain areas innervated by monamines and brain circuitry involved in inputs and outputs of these areas. The recent approval of esketamine as a rapid-acting antidepressant drug in treatment-resistant depression, has definitively projected glutamatergic transmission as a key constituent in the use of new drugs in antidepressant therapy. In this review we have examined the role of several brain areas: namely, the hippocampus, the medial Prefrontal Cortex (mPFC), the nucleus accumbens (NAc), the Lateral Habenula (LHb), the amygdala and the Bed Nucleus of Stria Terminalis (BNST). The reason for undertaking an in-depth review is due to their significant role in animal models of depression, which highlight their inter-connections as well as their inputs and outputs. In particular, we examined the modification of the expression and release of the brain derived neurotrophic factor (BDNF) and associated changes in dendritic density induced by chronic stress in the above areas of animal models of depression (AnMD). We also examined the effectiveness of ketamine and standard antidepressants in reversing these alterations, with the aim of identifying a brain circuit where pathological alteration might trigger the appearance of depression symptoms. Based on the role that these brain areas play in the generation of the symptoms of depression, we assumed that the mPFC, the NAc/Ventral Tegmental Area (VTA) and the hippocampus form a primary circuit of depression, where regular performance can endure resilience to stress. We have also examined how this circuit is affected by environmental challenges and how the activation of one or more areas, including amygdala, LHb or BNST can produce local detrimental effects that spread over specific circuits and generate depression symptoms. Furthermore, we also examined how, through their outputs, these three areas can negatively influence the NAc/VTA-PFC circuit directly or through the BNST, to generate anhedonia, one of the most devastating symptoms of depression.

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“…In humans, increased levels of pro-inflammatory cytokine IL-1, associated with reduced levels of hippocampal neurogenesis, have been reported in depressed patients and in animal models of depression [ 106 , 107 ]. Identifying the mechanisms by which inflammatory cytokines block neurogenesis in the human brain may provide insight that can be used to manage inflammation-associated mental health disorders, including diet, new diagnostic methods, and treatment therapies for depression [ 108 , 109 , 110 ].…”

Section: The Tryptophan–kynurenine Metabolic Systemmentioning

confidence: 99%

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan–Kynurenine Metabolic System

Tanaka

Szabó

Spekker

et al. 2022

Cells

123

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Nearly half a century has passed since the discovery of cytoplasmic inheritance of human chloramphenicol resistance. The inheritance was then revealed to take place maternally by mitochondrial DNA (mtDNA). Later, a number of mutations in mtDNA were identified as a cause of severe inheritable metabolic diseases with neurological manifestation, and the impairment of mitochondrial functions has been probed in the pathogenesis of a wide range of illnesses including neurodegenerative diseases. Recently, a growing number of preclinical studies have revealed that animal behaviors are influenced by the impairment of mitochondrial functions and possibly by the loss of mitochondrial stress resilience. Indeed, as high as 54% of patients with one of the most common primary mitochondrial diseases, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) syndrome, present psychiatric symptoms including cognitive impairment, mood disorder, anxiety, and psychosis. Mitochondria are multifunctional organelles which produce cellular energy and play a major role in other cellular functions including homeostasis, cellular signaling, and gene expression, among others. Mitochondrial functions are observed to be compromised and to become less resilient under continuous stress. Meanwhile, stress and inflammation have been linked to the activation of the tryptophan (Trp)–kynurenine (KYN) metabolic system, which observably contributes to the development of pathological conditions including neurological and psychiatric disorders. This review discusses the functions of mitochondria and the Trp-KYN system, the interaction of the Trp-KYN system with mitochondria, and the current understanding of the involvement of mitochondria and the Trp-KYN system in preclinical and clinical studies of major neurological and psychiatric diseases.

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Association between increased inflammatory cytokine expression in the lateral habenular nucleus and depressive-like behavior induced by unpredictable chronic stress in rats

Cited by 15 publications

References 41 publications

Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression

Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression

BDNF Alterations in Brain Areas and the Neurocircuitry Involved in the Antidepressant Effects of Ketamine in Animal Models, Suggest the Existence of a Primary Circuit of Depression

Mitochondrial Impairment: A Common Motif in Neuropsychiatric Presentation? The Link to the Tryptophan–Kynurenine Metabolic System

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