Chronic administration of glucocorticoid receptor ligands increases anxiety-like behavior and selectively increase serotonin transporters in the ventral hippocampus

Scholl, Jamie L.; Solanki, Rajeshwari R.; Watt, Michael J.; Renner, Kenneth J.; Forster, Gina L.

doi:10.1016/j.brainres.2022.148189

Cited by 4 publications

(4 citation statements)

References 82 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In clinical practice, TDS is less effective as a single dose than DZP and more effective when administered chronically; the results of this study appear to reflect this clinical fact 57 . Activation of GR in the PFC, hypothalamus, amygdala, and ventral hippocampus is known to induce anxiety-like behaviors via diverse mechanisms [12][13][14][15] . DSS-treated mice showed increased phosphorylation levels of GR in the PFC and ventral hippocampus (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…In animal studies, intraperitoneal administration of LPS has been reported to act on the adrenal cortex and increase blood corticosterone levels, resulting in anxiety-like behavior 9 – 11 . Hyperactivation in the brain of the glucocorticoid receptor (GR), a receptor for corticosterone, is implicated in the development of anxiety-like behavior 12 – 15 . From these findings, it can be surmised that gut microbiota imbalance may adversely affect the brain through elevated serum LPS and corticosterone, leading to anxiety symptoms.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Anxiolytic effects of Enterococcus faecalis 2001 on a mouse model of colitis

Takahashi,

Tsuji,

Nakagawasai

et al. 2024

Sci Rep

View full text Add to dashboard Cite

Ulcerative colitis (UC) is a refractory inflammatory bowel disease, which is known to cause psychiatric disorders such as anxiety and depression at a high rate in addition to peripheral inflammatory symptoms. However, the pathogenesis of these psychiatric disorders remains mostly unknown. While prior research revealed that the Enterococcus faecalis 2001 (EF-2001) suppressed UC-like symptoms and accompanying depressive-like behaviors, observed in a UC model using dextran sulfate sodium (DSS), whether it has an anxiolytic effect remains unclear. Therefore, we examined whether EF-2001 attenuates DSS-induced anxiety-like behaviors. Treatment with 2% DSS for seven days induced UC-like symptoms and anxiety-like behavior through the hole-board test, increased serum lipopolysaccharide (LPS) and corticosterone concentration, and p-glucocorticoid receptor (GR) in the prefrontal cortex (PFC), and decreased N-methyl-d-aspartate receptor subunit (NR) 2A and NR2B expression levels in the PFC. Interestingly, these changes were reversed by EF-2001 administration. Further, EF-2001 administration enhanced CAMKII/CREB/BDNF-Drebrin pathways in the PFC of DSS-treated mice, and labeling of p-GR, p-CAMKII, and p-CREB showed colocalization with neurons. EF-2001 attenuated anxiety-like behavior by reducing serum LPS and corticosterone levels linked to the improvement of UC symptoms and by facilitating the CAMKII/CREB/BDNF-Drebrin pathways in the PFC. Our findings suggest a close relationship between UC and anxiety.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anxiolytic effects of Enterococcus faecalis 2001 on a mouse model of colitis

Takahashi,

Tsuji,

Nakagawasai

et al. 2024

Sci Rep

View full text Add to dashboard Cite

show abstract

“…In line with previous studies, in this research, the injury of hippocampal structure and function exhibited depressive-like behaviors, as evidenced SPT, TST, and NSFT tests. Additionally, the deficiency in hippocampal activity is required for anxiety-like behaviors ( Chen et al, 2022 ; Scholl et al, 2022 ). Some studies reported by other groups have indicated that anxiety-like behaviors could be generated through ischemic/reperfusion injury ( Jin et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture treatment ameliorates depressive-like behavior and cognitive dysfunction via CB1R dependent mitochondria biogenesis after experimental global cerebral ischemic stroke

Zhou

Wang

et al. 2023

Front. Cell. Neurosci.

View full text Add to dashboard Cite

IntroductionThis study aimed to identify the effect of electroacupuncture (EA) treatment on post-stroke depression (PSD) and explore whether cannabinoid receptor 1 (CB1R)-mediated mitochondrial biogenesis accounts for the treatment effect of EA.MethodsThe PSD mouse model was induced by a consecutive 14-day chronic unpredictable stress operation after 7 days of recovery from the bilateral common carotid artery occlusion surgery. Either EA treatment or sham stimulation was performed for 14 consecutive days from Day 7 after the BCCAO operation. Subjects’ PSD-like behaviors were tested via open field test, sucrose preference test, novelty suppressed feeding test, tail suspension test, and forced swim test, and subjects’ cognitive function was examined using Y-maze and novelty object recognition test. In addition, the levels of CB1R, mitochondrial biogenesis-related proteins (nuclear transcription factor 1, NRF1; mitochondrial transcription factor A, TFAM), proteins related to mitochondrial function (Cytochrome C, Cyto C; AIF, COX IV), and mitochondrial DNA were measured. To elucidate the role of CB1R in EA treatment, CB1R antagonists AM251 and CB1R-shRNA were given to mice before EA treatment. Likewise, subjects’ depressive-like behaviors, cognitive function, mitochondrial function, and mitochondrial biogenesis were examined after the PSD procedure.ResultsIt has been showed that EA successfully ameliorated depressive-like behaviors, improved cognitive dysfunctions, and upregulated CB1R, NRF1 and TFAM expressions. However, the supplementation of AM251 and CB1R-shRNA blocked the antidepressant-like effects generated by EA, and EA failed to improve cognitive dysfunction, upregulate CB1R protein expression, and increase mitochondrial function and biogenesis.ConclusionAltogether, these results indicated that EA ameliorated PSD-like behaviors in mice, improved cognitive dysfunctions after PSD, and promoted mitochondrial biogenesis by activating CB1R, a novel mechanism underlying EA’s antidepressant-like effects in treating PSD.

show abstract

“…The glucocorticoid and serotoninergic systems are widely acknowledged as exerting a pivotal influence on the development of anxiety and depression [ 1 , 2 , 3 , 4 ]. Modifications in glucocorticoid synthesis and release or alterations in the composition of serotonin receptors across various cell subtypes within limbic and thalamocortical brain regions inevitably impact mental states [ 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

Prenatal Hypoxia Triggers a Glucocorticoid-Associated Depressive-like Phenotype in Adult Rats, Accompanied by Reduced Anxiety in Response to Stress

Stratilov,

Potapova,

Safarova

et al. 2024

IJMS

View full text Add to dashboard Cite

Fetal hypoxia and maternal stress frequently culminate in neuropsychiatric afflictions in life. To replicate this condition, we employed a model of prenatal severe hypoxia (PSH) during days 14–16 of rat gestation. Subsequently, both control and PSH rats at 3 months old were subjected to episodes of inescapable stress to induce learned helplessness (LH). The results of the open field test revealed an inclination towards depressive-like behavior in PSH rats. Following LH episodes, control (but not PSH) rats displayed significant anxiety. LH induced an increase in glucocorticoid receptor (GR) levels in extrahypothalamic brain structures, with enhanced nuclear translocation in the hippocampus (HPC) observed both in control and PSH rats. However, only control rats showed an increase in GR nuclear translocation in the amygdala (AMG). The decreased GR levels in the HPC of PSH rats correlated with elevated levels of hypothalamic corticotropin-releasing hormone (CRH) compared with the controls. However, LH resulted in a reduction of the CRH levels in PSH rats, aligning them with those of control rats, without affecting the latter. This study presents evidence that PSH leads to depressive-like behavior in rats, associated with alterations in the glucocorticoid system. Notably, these impairments also contribute to increased resistance to severe stressors.

show abstract

Chronic administration of glucocorticoid receptor ligands increases anxiety-like behavior and selectively increase serotonin transporters in the ventral hippocampus

Cited by 4 publications

References 82 publications

Anxiolytic effects of Enterococcus faecalis 2001 on a mouse model of colitis

Anxiolytic effects of Enterococcus faecalis 2001 on a mouse model of colitis

Electroacupuncture treatment ameliorates depressive-like behavior and cognitive dysfunction via CB1R dependent mitochondria biogenesis after experimental global cerebral ischemic stroke

Prenatal Hypoxia Triggers a Glucocorticoid-Associated Depressive-like Phenotype in Adult Rats, Accompanied by Reduced Anxiety in Response to Stress

Contact Info

Product

Resources

About