Electroconvulsive shock restores the decreased coverage of brain blood vessels by astrocytic endfeet and ameliorates depressive-like behavior

Azis, Ilhamuddin Abdul; Hashioka, Sadayuki; Tsuchie, Keiko; Miyaoka, Tsuyoshi; Abdullah, Rostia Arianna; Limoa, Erlyn; Arauchi, Ryosuke; Inoue, Ken; Miura, Shingo; Izuhara, Muneto; Kanayama, Misako; Otsuki, Koji; Nagahama, Michiharu; Kawano, Kiminori; Araki, Toshimitsu; Hayashida, Maiko; Wake, Rei; Oh‐Nishi, Arata; Tanra, Andi Jayalangkara; Horiguchi, Jun; Inagaki, Masumi

doi:10.1016/j.jad.2019.07.008

Cited by 18 publications

(10 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AQP4 is the principal water channel in the central nervous system (CNS), specifically localized to astrocyte end feet 37,38 to maintain BBB integrity 37 . Recent data suggest a role for AQP4 in the pathophysiology of mood disorders, 38 including alteration of brain AQP4 expression in mood disorders patients, 39 reduction in blood vessels coverage by AQP4‐immunoreactive astrocyte, 8,40 and association of genetic variation at AQP4 locus with vascular depression 41 . While Kon et al 42 previously showed increased hippocampal AQP4 expression under CMS, Xia et al 25 detected reduced expression of hippocampal AQP4 expression under CMS conditions.…”

Section: Discussionmentioning

confidence: 99%

Regulatory effect of lithium on hippocampal blood‐brain barrier integrity in a rat model of depressive‐like behavior

Taler

Aronovich²,

Hornfeld³

et al. 2020

Bipolar Disorders

View full text Add to dashboard Cite

Objectives Recent evidence has associated mood disorders with blood‐brain barrier (BBB)/ neurovascular unit (NVU) dysfunction, and reduction in blood vessels coverage by the water channel aquaporin‐4 (AQP4) immunoreactive astrocytes. Lithium is an established treatment for mood disorders, yet, its mechanism of action is partially understood. We investigated the effects of lithium on BBB integrity and NVU‐related protein expression in chronic mild stress (CMS) rat model of depressive‐like behavior. Methods Male Wistar rats were exposed for 5 weeks to unpredictable mild stressors with daily co‐administration of lithium chloride to half of the stressed and unstressed groups. Sucrose preference and open field tests were conducted to validate the depressive‐like phenotype, and dynamic contrast‐enhanced MRI analysis was utilized to assess BBB integrity in brain regions relevant to the pathophysiology of depression. Hippocampal AQP4 and claudin‐5 expression were studied using immunofluorescence, western blot, and enzyme‐linked immunosorbent assays. Results Lithium administration to the stressed rats prevented the reductions in sucrose preference and distance traveled in the open field, and normalized the stress‐induced hippocampal BBB hyperpermeability, whereas lithium administration to the unstressed rats increased hippocampal BBB permeability. Additionally, lithium treatment attenuated the decrease in hippocampal AQP4 to glial fibrillary acidic protein immunoreactivity ratio in the stressed rats and upregulated hippocampal claudin‐5 and BDNF proteins expression. Conclusions Our findings suggest that lithium administration in a rat CMS model of depressive‐like behavior is associated with attenuation of stressed‐induced hippocampal BBB/NVU disruption. These protective effects may be relevant to the mode of action of lithium in depression.

show abstract

Section: Discussionmentioning

confidence: 99%

Regulatory effect of lithium on hippocampal blood‐brain barrier integrity in a rat model of depressive‐like behavior

Taler

Aronovich²,

Hornfeld³

et al. 2020

Bipolar Disorders

View full text Add to dashboard Cite

show abstract

“…Although spatial recognition memory was not definitively impaired, spatial mobilization was decreased in the 4-week DEP group. Such immobility is suggestive of depressive behavior 10–12 . These changes became normalized after 8 weeks of DEP exposure.…”

Section: Discussionmentioning

confidence: 99%

Neuronal and perineuronal changes of cerebral cortex after exposure to inhaled particulate matter

Kim

Lee

Park

et al. 2019

Sci Rep

View full text Add to dashboard Cite

The inhalation of particulate matter (PM) increases the perineuronal nets (PNNs) in the cerebral cortex; however, little is known about the related molecular changes. We explored how PM exposure impacted cognitive function and the levels of PNN-related genes. BALB/c mice (6-week-old females, n = 32) were exposed to 1–5-μm diesel-extracted particles (DEPs) (100 µg/m3, 5 hours per day, 5 days per week) and categorized into the following four groups: 1) 4-week DEP exposure (n = 8); 2) 4-week control (n = 8); 3) 8-week DEP exposure (n = 8); and 4) 8-week control (n = 8). The Y-maze test and olfactory function test were conducted after 4 and 8 weeks of DEP exposure. The prefrontal cortex, olfactory bulb and temporal cortex were harvested from the animals in each group. The expression of genes related to PNNs (Tenascin C, matrix metalloproteinase [MMP]14, MMP9) and synaptic vesicular transporters of vesicular glutamergic transporter 1 (VGLUT1), VGLUT2, vesicular GABAergic transporter (VGAT) were measured. The temporal cortex was immunostained for neurocan, VGLUT1, and VGAT. The 4-week DEP group had lower total arm entry in the Y-maze test and olfactory sensitivity. These impaired behavioral functions recovered in the 8-week DEP group. Expression of tenascin C and MMP9 were increased in the cerebral cortex in the 8-week DEP group compared with the control group. The levels of VGLUT1, VGLUT2, and VGAT were elevated in the cerebral cortex of the 8-week DEP group compared with the control group. In immunostaining of the temporal cortex, the expression of neurocan, VGLUT1, and GAD67 were increased in the 8-week DEP group compared with the control group. The 4-week DEP inhalation impaired spatial activities and olfactory sensitivities. After 8 weeks of DEP exposure, the PNN components and their proteolytic enzymes and the vesicular transporters increased in the cerebral cortex.

show abstract

“…Electroconvulsive therapy (ECT) was claimed to be an effective treatment for depression ( Rasmussen, 2011 ; Azis et al, 2019 ). Likewise, ECT has been discovered to trigger the gene Gadd45b, which plays a part in BDNF demethylation in the dentate gyrus of the hippocampus formation ( Ma et al, 2009 ).…”

Section: The Role Of Gadd45b In Neuropsychiatric Disordersmentioning

confidence: 99%

The role of Gadd45b in neurologic and neuropsychiatric disorders: An overview

Shen

Shi

et al. 2022

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Growth arrest and DNA damage-inducible beta (Gadd45b) is directly intertwined with stress-induced DNA repair, cell cycle arrest, survival, and apoptosis. Previous research on Gadd45b has focused chiefly on non-neuronal cells. Gadd45b is extensively expressed in the nervous system and plays a critical role in epigenetic DNA demethylation, neuroplasticity, and neuroprotection, according to accumulating evidence. This article provided an overview of the preclinical and clinical effects of Gadd45b, as well as its hypothesized mechanisms of action, focusing on major psychosis, depression, autism, stroke, seizure, dementia, Parkinson’s disease, and autoimmune diseases of the nervous system.

show abstract

Electroconvulsive shock restores the decreased coverage of brain blood vessels by astrocytic endfeet and ameliorates depressive-like behavior

Cited by 18 publications

References 44 publications

Regulatory effect of lithium on hippocampal blood‐brain barrier integrity in a rat model of depressive‐like behavior

Regulatory effect of lithium on hippocampal blood‐brain barrier integrity in a rat model of depressive‐like behavior

Neuronal and perineuronal changes of cerebral cortex after exposure to inhaled particulate matter

The role of Gadd45b in neurologic and neuropsychiatric disorders: An overview

Contact Info

Product

Resources

About