ArticleScientific reports2018
Stably maintained microtubules protect dopamine neurons and alleviate depression-like behavior after intracerebral hemorrhage.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
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- Cardiovascular disease and depression: a bidirectional relationship and its clinical implications.Frontiers in psychiatry · 2025Review
- Selective HDAC6 inhibition protects against blood-brain barrier dysfunction after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- Cyclophilin D-induced mitochondrial impairment confers axonal injury after intracerebral hemorrhage in mice.Neural regeneration research · 2023Article
- A novel aged mouse model of recurrent intracerebral hemorrhage in the bilateral striatum.Neural regeneration research · 2023Article
- Acupuncture treatment for post-stroke depression: Intestinal microbiota and its role.Frontiers in neuroscience · 2023Review
- Blood-Brain Barrier Dysfunction in the Pathogenesis of Major Depressive Disorder.Cellular and molecular neurobiology · 2022Review
- Article
- Potential Genes and Mechanisms Linking Intracerebral Hemorrhage and Depression: A Bioinformatics-Based Study.International journal of general medicine · 2021Article
- Quantitative Iron Neuroimaging Can Be Used to Assess the Effects of Minocycline in an Intracerebral Hemorrhage Minipig Model.Translational stroke research · 2020Article
- Article
- Heterogeneity of dopamine release sites in health and degeneration.Neurobiology of disease · 2020Review
- Protracted Morphological Changes in the Corticospinal Tract Within the Cervical Spinal Cord After Intracerebral Hemorrhage in the Right Striatum of Mice.Frontiers in neuroscience · 2020Article
- DRG2 Deficient Mice Exhibit Impaired Motor Behaviors with Reduced Striatal Dopamine Release.International journal of molecular sciences · 2019Article
- Epothilone B Benefits Nigral Dopaminergic Neurons by Attenuating Microglia Activation in the 6-Hydroxydopamine Lesion Mouse Model of Parkinson's Disease.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesolimbic dopamine (DA) system lesion plays a key role in the pathophysiology of depression, and our previous study demonstrated that reduced microtubule (MT) stability aggravated nigrostriatal pathway impairment after intracerebral hemorrhage (ICH). This study aimed to further investigate the occurrence regularity of depression-like behavior after ICH and determine whether maintaining MT stabilization could protect DA neurons in ventral tegmental area (VTA) and alleviate depression-like behavior after ICH. An intrastriatal injection of 20 μl of autologous blood or MT depolymerization reagent nocodazole (Noco) was used to mimic the pathology of ICH model in mice. The concentration of DA, number of DA neurons and acetylated α-tubulin (a marker for stable MT) in VTA were checked, and depression-related behavior tests were performed after ICH. A MT-stabilizing agent, epothilone B (EpoB), was administered to explore the effects of MT stabilization on DA neurons and depression-like behavior after ICH. The results showed that obvious depression-like behavior occurred at 7, 14, and 28 days (P < 0.01) after ICH. These time-points were related to significant decreases in the concentration of DA (P < 0.01) and number of DA neurons (P < 0.01) in VTA. Moreover, The decrease of acetylated α-tubulin expression after ICH and Noco injection contributed to DA neurons' impairment in VTA, and Noco injecton also aggravate ICH-induced depression-like behaviors and DA neurons' injury. Furthermore, EpoB treatment significantly ameliorated ICH and Noco-induced depression-like behaviors (P < 0.05) and increased the concentration of DA (P < 0.05) and number of DA neurons (P < 0.05) in VTA by increasing the level of acetylated α-tubulin. The results indicate that EpoB can protect DA neurons by enhancing MT stability, and alleviate post-ICH depressive behaviors. This MT-targeted therapeutic strategy shows promise as a bench-to-bedside translational method for treating depression after ICH.
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