Wuling Capsule promotes hippocampal neurogenesis by improving expression of connexin 43 in rats exposed to chronic unpredictable mild stress

Li, Deqiang; Li, Xujuan; Duan, Jin-feng; Cai, Wei

doi:10.3736/jcim20100710

Cited by 17 publications

(12 citation statements)

References 20 publications

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“…Furthermore, in a model of major depressive disorder, Menard et al ( 14 ) reported that Cldn5, a standard BBB marker, was altered. Li et al ( 40 ) also reported that connexin 40, which is a gap junction protein and an indicator of astrocytic population general health, was altered in chronic mildly stressed rats. It was additionally determined that oral administration of fluoxetine reversed these changes.…”

Section: Discussionmentioning

confidence: 98%

Examining the central effects of chronic stressful social isolation on rats

et al. 2020

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Stress-related disorders are extremely complex and current treatment strategies have limitations. The present study investigated alternative pathological mechanisms using a combination of multiple environmental approaches with biochemical and molecular tools. The aim of the present study was to evaluate blood-brain-barrier (BBB) integrity in socially manipulated animal housing conditions. Multiple environmentally-related models were employed in the current study. The main model proposed (chronically isolated rats) was biochemically validated using the level of peripheral corticosterone. The current study examined and compared the mRNA levels of certain inflammatory and BBB markers in the hippocampal tissue of chronically isolated rats, including claudin-5 ( cldn5 ) and tight junction protein ( tjp ). Animals were divided into four groups: i) Standard housed rats (controls); ii) chronically isolated rats; iii) control rats treated with fluoxetine, which is a standard selective serotonin reuptake inhibitor; and iv) isolated rats treated with fluoxetine. To further examine the effect of environmental conditions on BBB markers, the current study assessed BBB markers in enriched environmental (EE) housing and short-term isolation conditions. The results demonstrated a significant increase in cldn5 and tjp levels in the chronically isolated group. Despite some anomalous results, alterations in mRNA levels were further confirmed in EE housing conditions compared with chronically isolated rats. This trend was also observed in rats subjected to short-term isolation compared with paired controls. Additionally, levels of IL-6, an inflammatory marker associated with neuroinflammation, were markedly increased in the isolated group. However, treatment with fluoxetine treatment reversed these effects. The results indicated that BBB integrity may be compromised in stress-related disorders, highlighting a need for further functional studies on the kinetics of BBB in stress-related models.

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Section: Discussionmentioning

confidence: 98%

Examining the central effects of chronic stressful social isolation on rats

et al. 2020

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“…Previous studies indicated that the molecular mechanism of the antidepressant effect of Wuling capsule was related to the improvement of the low hippocampal neurogenesis in rats subjected to chronic unpredictable mild stress (CMS), and the antidepressant effects are related to enhancing the Cx43 expression but not through BDNF mediation (Li et al, 2010). Furthermore, Wuling capsule has been shown to improve the cognitive deficits and response rate of anti-depression in PSD rats, but the mechanisms of Wuling capsule improving the impairments of learning and memory in PSD rats are not mediated by BDNF (Li et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Wuling powder prevents the depression-like behavior in learned helplessness mice model through improving the TSPO mediated-mitophagy

Zheng

Wang

et al. 2016

Journal of Ethnopharmacology

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“…Alteration in the Cx43 mRNA and protein levels have also been observed in the PFC (Sun, Liu, Yuan, Li, & Chen, ) and hippocampus (Li, Li, Duan, & Cai, ) in animal models of depression. In rats with CMS‐induced depression, the expression levels of Cx43 mRNA and protein were reduced in the hippocampus, and were restored to normal levels through a BDNF‐independent pathway with the treatment of a compound traditional Chinese herbal medicine with antidepressant activity (Li et al, ). Another group reported similar findings in the PFC, and treatment with the typical antidepressant fluoxetine reversed the reductions in the diffusion of a gap junction channel‐permeable dye and Cx43 expression in rats subjected to CMS (Sun et al, ).…”

Section: Gap Junctionsmentioning

confidence: 99%

“…Although prolonged corticosterone exposure elicited anxiety and depression‐like behaviors and increased Cx43 phosphorylation in the hippocampus, chronic administration of fluoxetine reversed these behavioral and molecular abnormalities, suggesting that fluoxetine may exert its therapeutic effect by decreasing the expression or activity of Cx43 in the hippocampus (Quesseveur et al, ). It is currently unknown what accounts for the inconsistency (Li et al, ; Quesseveur et al, ). Thus, although astrocytic gap junctions may represent a novel potential therapeutic target for the treatment of patients with MDD (Sarrouilhe and Dejean, ), more preclinical and clinical experiments are required to test this idea in the future.…”

Section: Gap Junctionsmentioning

confidence: 99%

An astroglial basis of major depressive disorder? An overview

Wang

Jie

Liu

et al. 2017

Glia

172

125

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Depression is a chronic, recurring, and serious mood disorder that afflicts up to 20% of the global population. The monoamine hypothesis has dominated our understanding of the pharmacotherapy of depression for more than half a century; however, our understanding of the pathophysiology and pathogenesis of major depression has lagged far behind. Astrocytes are the most abundant and versatile cells in the brain, participating in most, if not all, of brain functions as both a passive housekeeper and an active player. Mounting evidence from clinical, preclinical and post-mortem studies has revealed a decrease in the number or density of astrocytes and morphological and functional astroglial atrophy in patients with major depressive disorder (MDD) and in animal models of depression. Furthermore, currently available antidepressant treatments at least partially exert their therapeutic effects on astrocytes. More importantly, dysfunctional astrocytes lead to depressive-like phenotypes in animals. Together, current studies point to astroglial pathology as the potential root cause of MDD. Thus, a shift from a neuron-centric to an astrocyte-centric cause of MDD has gained increasing attention during the past two decades. Here we will summarize the current evidence supporting the hypothesis that MDD is a disease of astrocyte pathology and highlight previous studies on promising strategies that directly target astrocytes for the development of novel antidepressant treatments.

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Wuling Capsule promotes hippocampal neurogenesis by improving expression of connexin 43 in rats exposed to chronic unpredictable mild stress

Cited by 17 publications

References 20 publications

Examining the central effects of chronic stressful social isolation on rats

Examining the central effects of chronic stressful social isolation on rats

Wuling powder prevents the depression-like behavior in learned helplessness mice model through improving the TSPO mediated-mitophagy

An astroglial basis of major depressive disorder? An overview

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