Neonatal Proinflammatory Stress and Expression of Neuroinflammation-Associated Genes in the Rat Hippocampus

Kvichansky, A. A.; Tret’yakova, L. V.; Volobueva, Maria N; Manolova, Anna; Stepanichev, M. Yu.; Онуфриев, М. В.; Moiseeva, Yulia; Лазарева, Н. А.; Bolshakov, A D; Gulyaeva, N. V.

doi:10.1134/s0006297921060079

Cited by 3 publications

(10 citation statements)

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“…Neuroplasticity is defined as the brain’s ability to undergo neurobiological changes in response to extrinsic stimuli such as early life adversity 5 - 7 and chronic exposure to stress 8 , 9 and/or intrinsic stimuli most notably genetic or epigenetic effects 10 , 11 . The responses to these changes can be visualized at a structural level (e.g., cell number, dendritic spine density and morphology or synaptic protein levels) and at a functional level (e.g., synchronous firing) that in turn determine the state of networks 12 , 13 , stress responses, mood, cognition and behavior.…”

Section: Introductionmentioning

confidence: 99%

Dysregulation of adult hippocampal neuroplasticity in major depression: pathogenesis and therapeutic implications

et al. 2022

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Major depressive disorder (MDD) was previously hypothesized to be a disease of monoamine deficiency in which low levels of monoamines in the synaptic cleft were believed to underlie depressive symptoms. More recently, however, there has been a paradigm shift towards a neuroplasticity hypothesis of depression in which downstream effects of antidepressants, such as increased neurogenesis, contribute to improvements in cognition and mood. This review takes a top-down approach to assess how changes in behavior and hippocampal-dependent circuits may be attributed to abnormalities at the molecular, structural and synaptic level. We conclude with a discussion of how antidepressant treatments share a common effect in modulating neuroplasticity and consider outstanding questions and future perspectives.

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Section: Introductionmentioning

confidence: 99%

Dysregulation of adult hippocampal neuroplasticity in major depression: pathogenesis and therapeutic implications

et al. 2022

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“…cortex (Berkiks et al, 2018b,a) along with normal levels of IL-6 (Kvichansky et al, 2021; Table 5). Notably, mRNA levels of these cytokines show the opposite directions of alterations: Tnf mRNA expression is unchanged, whereas Il-6 mRNA expression is elevated in the hippocampus of males (Kvichansky et al, 2021).…”

Section: Frontiers Inmentioning

confidence: 99%

“…Importantly, only one study points to a link between microglial activation and the development of depressive behavior in adolescence (postnatal days 35-42; Cao et al, 2021). In other studies, on animals of this age, investigators find either microglial activation without the development of depressive behavior (Lei et al, 2017) or depressive behavior not accompanied by microglial activation (Kvichansky et al, 2021).…”

Section: Microgliamentioning

confidence: 99%

“…Accordingly, the absence of any changes in levels of cytokines in blood plasma either at baseline or after stress, together with the imbalance of cytokines in brain tissues, indicates long-term persistence of local inflammation, which is accompanied by the development of depressive behavior too. It should also be noted that in adult females, the basal level of TNF, just as the magnitude of microglial activation (Berkiks et al, 2019b;Kvichansky et al, 2021) and the level of oxidative stress (Benmhammed et al, 2019), is higher than that in males (Berkiks et al, 2019b). Nonetheless, after 11 months, it is females with depression-like behavior who show an increased concentration of TNF in the prefrontal cortex (Berkiks et al, 2019a), whereas in males, this concentration does not differ from the level of control females and between control males and males with a history of NIA.…”

Section: Frontiers Inmentioning

confidence: 99%

“…One of the simple experimental approaches to the research on the influence of the immune system on the developing brain is to induce antibacterial immune responses without direct administration of bacterial pathogens, i.e., via injection of bacterial endotoxin: lipopolysaccharide (LPS). The use of the mimetic rather than a live bacterium has a number of advantages: biological safety, dose-dependent intensity of the immune response (Furube et al, 2018 ), and the ability to quantify cytokines (Yan and Kentner, 2017 ; Custódio et al, 2018 ; Berkiks et al, 2019a ) and the expression of immune-system–related genes (Cao et al, 2021 ; Kvichansky et al, 2021 ) in the blood and various tissues, including the brain. Additionally, the effect of mimetic administration is time-limited: 24–48 h depending on the dose (Furube et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

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Once induced, it lasts for a long time: the structural and molecular signatures associated with depressive-like behavior after neonatal immune activation

Khantakova

Bondar

Antontseva

et al. 2022

Front. Cell. Neurosci.

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Adverse factors such as stress or inflammation in the neonatal period can affect the development of certain brain structures and have negative delayed effects throughout the lifespan of an individual, by reducing cognitive abilities and increasing the risk of psychopathologies. One possible reason for these delayed effects is the neuroinflammation caused by neonatal immune activation (NIA). Neuroinflammation can lead to disturbances of neurotransmission and to reprogramming of astroglial and microglial brain cells; when combined, the two problems can cause changes in the cytoarchitecture of individual regions of the brain. In addition, neuroinflammation may affect the hypothalamic–pituitary–adrenal (HPA) axis and processes of oxidative stress, thereby resulting in higher stress reactivity. In our review, we tried to answer the questions of whether depressive-like behavior develops after NIA in rodents and what the molecular mechanisms associated with these disorders are. Most studies indicate that NIA does not induce depressive-like behavior in a steady state. Nonetheless, adult males (but not females or adolescents of both sexes) with experience of NIA exhibit marked depressive-like behavior when exposed to aversive conditions. Analyses of molecular changes have shown that NIA leads to an increase in the amount of activated microglia and astroglia in the frontal cortex and hippocampus, an increase in oxidative-stress parameters, a change in stress reactivity of the HPA axis, and an imbalance of cytokines in various regions of the brain, but not in blood plasma, thus confirming the local nature of the inflammation. Therefore, NIA causes depressive-like behavior in adult males under aversive testing conditions, which are accompanied by local inflammation and have sex- and age-specific effects.

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Ambiguous Contribution of Glucocorticosteroids to Acute Neuroinflammation in the Hippocampus of Rat

Tret’yakova,

Kvichansky,

Barkovskaya

et al. 2023

IJMS

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Effects of modulation of glucocorticoid and mineralocorticoid receptors (GR and MR, respectively) on acute neuroinflammatory response were studied in the dorsal (DH) and ventral (VH) parts of the hippocampus of male Wistar rats. Local neuroinflammatory response was induced by administration of bacterial lipopolysaccharide (LPS) to the DH. The modulation of GR and MR was performed by dexamethasone (GR activation), mifepristone, and spironolactone (GR and MR inhibition, respectively). Experimental drugs were delivered to the dentate gyrus of the DH bilaterally by stereotaxic injections. Dexamethasone, mifepristone, and spironolactone were administered either alone (basal conditions) or in combination with LPS (neuroinflammatory conditions). Changes in expression levels of neuroinflammation-related genes and morphology of microglia 3 days after intrahippocampal administration of above substances were assessed. Dexamethasone alone induced a weak proinflammatory response in the hippocampal tissue, while neither mifepristone nor spironolactone showed significant effects. During LPS-induced neuroinflammation, GR activation suppressed expression of selected inflammatory genes, though it did not prevent appearance of activated forms of microglia. In contrast to GR activation, GR or MR inhibition had virtually no influence on LPS-induced inflammatory response. The results suggest glucocorticosteroids ambiguously modulate specific aspects of neuroinflammatory response in the hippocampus of rats at molecular and cellular levels.

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Neonatal Proinflammatory Stress and Expression of Neuroinflammation-Associated Genes in the Rat Hippocampus

Cited by 3 publications

References 45 publications

Dysregulation of adult hippocampal neuroplasticity in major depression: pathogenesis and therapeutic implications

Dysregulation of adult hippocampal neuroplasticity in major depression: pathogenesis and therapeutic implications

Once induced, it lasts for a long time: the structural and molecular signatures associated with depressive-like behavior after neonatal immune activation

Ambiguous Contribution of Glucocorticosteroids to Acute Neuroinflammation in the Hippocampus of Rat

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