Antidepressants and Neuroinflammation: Can Antidepressants Calm Glial Rage Down?

Hashioka, Sadayuki

doi:10.2174/138955711795906888

Cited by 46 publications

(33 citation statements)

References 53 publications

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“…[126][127][128] Mitochondrial perturbations have been linked to major depression 114,[129][130][131] and bipolar disorder. 129,130,132 Inflammation has also been associated with major depression 116,131,[133][134][135] and bipolar disorder. 132,[136][137][138] For example, sleep deprivation is thought to trigger an inflammatory and stress response in the brain through gene induction.…”

Section: Additional Heuristic Melatonergic Antidepressant and Anxiolymentioning

confidence: 99%

Agomelatine in Depressive Disorders: Its Novel Mechanisms of Action

Srinivasan¹,

Zakaria²,

Othman³

et al. 2012

JNP

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Disruptions in sleep and sleep-wake cycle regulation have been identified as one of the main causes for the pathophysiology of depressive disorders. The search has been on for the identification of an ideal antidepressant that could improve both sleep disturbances and depressive symptomatology. Melatonin, the major hormone of the pineal gland, has been shown to improve sleep and is involved in the regulation of the sleep-wake cycle. Identification of high concentrations of MT1 and MT2 melatonergic receptors in the suprachiasmatic nucleus of the anterior hypothalamus, the structure concerned with regulation of circadian rhythms and sleep-wake cycles, has led to the development of melatonergic agonists with greater potency and longer durations of action. Agomelatine is one such melatonergic agonist that acts specifically on MT1/MT2 melatonergic receptors and at the same time exhibits 5-HT2C antagonism, a property that is utilized by current antidepressants that are in clinical use. Agomelatine has been shown to be effective in a number of animal models of depression. Clinical studies undertaken on patients with major depression, bipolar disorders, seasonal affective disorder, and generalized anxiety disorder have all shown that agomelatine is also very effective in ameliorating depressive symptoms and manifesting early onset of action with a good tolerability and safety profile. It improved sleep efficiency and also resynchronized the disrupted circadian rhythms. Hence, the melatonergic modulation by agomelatine is suggested as one of the mechanisms for its antidepressant effect. Agomelatine's action on dendritic neurogenesis in animal models of depression is also identified as yet another action.

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Section: Additional Heuristic Melatonergic Antidepressant and Anxiolymentioning

confidence: 99%

Agomelatine in Depressive Disorders: Its Novel Mechanisms of Action

Srinivasan¹,

Zakaria²,

Othman³

et al. 2012

JNP

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“…Also in animal experiments, depressive behavioral abnormalities are observed in rats treated with lipopolysaccharide or pro‐inflammatory cytokines (Kelley et al., 2013; Yirmiya, 1996). Neuroinflammation can be considered to be a glial cell‐propagated inflammation (Hashioka, 2011). These observations prompted us to determine whether glial activated Gunn rats also show depression‐like behavior.…”

Section: Introductionmentioning

confidence: 99%

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

et al. 2018

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IntroductionRecent studies imply that glial activation plays a role in the pathogenesis of psychiatric disorders, such as schizophrenia and major depression. We previously demonstrated that Gunn rats with hyperbilirubinemia show congenital gliosis and schizophrenia‐like behavior.MethodsAs it has been suggested that major depression involves glial activation associated with neuroinflammation, we examined whether Gunn rats show depression‐like behavior using the forced swimming test (FST) and the tail suspension test (TST). In addition, we quantitatively evaluated both microgliosis and astrogliosis in the hippocampus of Gunn rats using immunohistochemistry analysis of the microglial marker ionized calcium‐binding adaptor molecule (Iba) 1 and the astrocytic marker S100B.ResultsBoth the FST and TST showed that immobility time of Gunn rats was significantly longer than that of normal control Wistar rats, indicating that Gunn rats are somewhat helpless, a sign of depression‐like behavior. In the quantification of immunohistochemical analysis, Iba1immunoreactivity in the dentate gyrus (DG), cornu ammonis (CA) 1, and CA3 and the number of Iba1‐positive cells in the CA1 and CA3 were significantly increased in Gunn rats compared to Wistar rats. S100B immunoreactivity in the DG, CA1, and CA3 and the number of S100B‐positive cells in the DG and CA3 were significantly increased in Gunn rats compared to Wistar rats.ConclusionOur findings suggest that both microglia and astrocyte are activated in Gunn rats and their learned helplessness could be related to glial activation.

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“…In addition, recent rodent studies have suggested that astrocytes modulate anxious and depressive behaviors (8, 9). On the other hand, direct modulating effects of antidepressants have also been revealed (10–13). Thus, astrocytes have been supposed to be a novel therapeutic target against various psychiatric disorders such as major affective disorders and bipolar disorders (14, 15).…”

Section: Glial Roles and Pathology In Psychiatric Disordersmentioning

confidence: 99%

Neuron-Glia Interaction as a Possible Glue to Translate the Mind-Brain Gap: A Novel Multi-Dimensional Approach Toward Psychology and Psychiatry (R1)

2013

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Neurons and synapses have long been the dominant focus of neuroscience, thus the pathophysiology of psychiatric disorders has come to be understood within the neuronal doctrine. However, the majority of cells in the brain are not neurons but glial cells including astrocytes, oligodendrocytes, and microglia. Traditionally, neuroscientists regarded glial functions as simply providing physical support and maintenance for neurons. Thus, in this limited role glia had been long ignored. Recently, glial functions have been gradually investigated, and increasing evidence has suggested that glial cells perform important roles in various brain functions. Digging up the glial functions and further understanding of these crucial cells, and the interaction between neurons and glia may shed new light on clarifying many unknown aspects including the mind-brain gap, and conscious-unconscious relationships. We briefly review the current situation of glial research in the field, and propose a novel translational research with a multi-dimensional model, combining various experimental approaches such as animal studies, in vitro & in vivo neuron-glia studies, a variety of human brain imaging investigations, and psychometric assessments.

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Antidepressants and Neuroinflammation: Can Antidepressants Calm Glial Rage Down?

Cited by 46 publications

References 53 publications

Agomelatine in Depressive Disorders: Its Novel Mechanisms of Action

Agomelatine in Depressive Disorders: Its Novel Mechanisms of Action

Gunn rats with glial activation in the hippocampus show prolonged immobility time in the forced swimming test and tail suspension test

Neuron-Glia Interaction as a Possible Glue to Translate the Mind-Brain Gap: A Novel Multi-Dimensional Approach Toward Psychology and Psychiatry (R1)

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