
Neuron, Journal Year: 2022, Volume and Issue: 110(7), P. 1116 - 1138
Published: Feb. 18, 2022
Language: Английский
Neuron, Journal Year: 2022, Volume and Issue: 110(7), P. 1116 - 1138
Published: Feb. 18, 2022
Language: Английский
Frontiers in Molecular Neuroscience, Journal Year: 2018, Volume and Issue: 11
Published: May 31, 2018
Depression is the second leading cause of disability worldwide. The effects clinical depression may be mediated by neuroinflammation such as activation microglia and high levels proinflammatory cytokines in certain brain areas. Traditional Chinese medicine techniques electro-acupuncture (EA) are used extensively Asia to treat mental health disorders. However, EA has not been rigorously studied treatment depression. This study was designed assess effectiveness on depressive-like behavior explore role hippocampal potential antidepressant effect EA. In this study, we 6 chronic unpredictable stressors daily a random sequence for 10 weeks. were performed 'Bai-Hui' (Du-20) (+) 'Yang-Ling-Quan' (GB-34, right side) (−) acupoints an apparatus (HANS Electronic Apparatus, LH202H, 2\100Hz, 0.3 mA) 30 mins once every other day last 4 tests including open field test forced swimming test, which widely depressive anxiety-like Monday Tuesday eleventh week. results showed that ten week stress (CUS) caused behavioral deficits rats hippocampus, increased expression NLRP3 inflammasome components, upregulated mRNA level IL-1β protein mature form (p17) microglia. Moreover, four weeks significantly attenuated CUS. EA's accompanied markedly decreased components matured IL-1β. Meanwhile, can reverse CUS-induced increases P2X7 receptor, Iba-1, IL-18, TNFα IL-6 decreases GFAP expression. conclusion, exhibited alleviated neuroinflammation. These findings provide insight into Key Words: depression; EA; stress; IL-1β; receptor; glia
Language: Английский
Citations
84Scientific Reports, Journal Year: 2019, Volume and Issue: 9(1)
Published: Feb. 28, 2019
Abstract With increasing prevalence, chronic kidney disease (CKD) has become a global health problem. Due to the retention of uremic toxins, electrolytes and water, resultant metabolic disturbances, CKD affects several organs, including nervous system. Thus, patients suffer from neurological complications, dementia, cognitive impairment, motor abnormalities, depression, mood sleep disturbances. However, mechanisms underlying complications are least elucidated. We have recently reported highly reproducible mice model induced by high adenine diet, which exhibited psychomotor behavioral abnormalities blood-brain barrier disruption. In present study, using model, we investigated psycho-motor behaviour, neurochemical histopathological alterations in brain relevant observed behavioural abnormalities. The results demonstrate loss Acetylcholinesterase activity, decrease neuronal arborisation dendritic spine density discrete regions, mice. Oxidative stress, inflammation, mitochondrial dysfunctions were found specific regions mice, been regarded as causes alterations. study is immense importance, therapeutic implications management CKD-associated complications.
Language: Английский
Citations
84Cell Reports, Journal Year: 2021, Volume and Issue: 36(6), P. 109508 - 109508
Published: Aug. 1, 2021
Astrocytic contributions to neuroinflammation are widely implicated in disease, but they remain incompletely explored. We assess medial prefrontal cortex (PFC) and visual (VCX) astrocyte whole-tissue gene expression changes mice following peripherally induced triggered by a systemic bacterial endotoxin, lipopolysaccharide, which produces sickness-related behaviors, including anhedonia. Neuroinflammation-mediated behavioral astrocyte-specific alterations peak when anhedonia is greatest then reverse normal. Notably, region-specific molecular identities of PFC VCX astrocytes largely maintained during reactivity changes. Gene pathway analyses reveal diverse cell signaling pathways, cell-cell interactions multiple types that may underlie the central effects neuroinflammation. Certain signatures accompanying shared with reported Alzheimer's disease mouse models. However, we find no evidence altered neuronal survival or function even neuroinflammation-induced significant.
Language: Английский
Citations
82Neuropsychopharmacology, Journal Year: 2022, Volume and Issue: 48(1), P. 21 - 36
Published: May 16, 2022
Language: Английский
Citations
56Neuron, Journal Year: 2022, Volume and Issue: 110(7), P. 1116 - 1138
Published: Feb. 18, 2022
Language: Английский
Citations
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