ArticleAnnals of clinical and translational neurology2021
The α2δ-1/NMDA receptor complex is involved in brain injury after intracerebral hemorrhage in mice.
Article in Annals of clinical and translational neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- [Benefits and risks of gabapentinoids in geriatric psychiatry].Der Nervenarzt · 2026Review
- Efficacy of pregabalin in the treatment of acute cerebral hemorrhage and its influence on prognosis.Frontiers in pharmacology · 2026Article
- Ion Channel Dysregulation Following Intracerebral Hemorrhage.Neuroscience bulletin · 2024Review
- Article
- The α2δ-1-NMDA receptor complex and its potential as a therapeutic target for ischemic stroke.Frontiers in neurology · 2023Review
- Intracerebral hemorrhage alters α2δ1 and thrombospondin expression in rats.Experimental and therapeutic medicine · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
backgroundIntracerebral hemorrhage (ICH), a common cerebrovascular disease, seriously threatens human health and has severe secondary injuries, while existing treatment methods have many limitations. α2δ-1 is a subunit of voltage-gated Ca
methodsWe first performed ICH modeling on WT mice and Cacna2d1 knockout (KO) mice. The expression levels of GluN1 and α2δ-1 were measured by Western blot and q-PCR, and the interaction between the two proteins was evaluated by co-precipitation. The neuronal apoptosis was detected by the TUNEL assay, and the expression levels of inflammatory factors were assessed by ELISA. The nerve functions of mice were evaluated using behavioral experiments including corner turn test and forelimb use asymmetry. Cerebral hematoma was indicated by brain water content and lesion volume.
resultsICH up-regulated the expression levels of α2δ-1 and GluN1. KO of Cacna2d1 significantly reduced the ICH-induced apoptosis. The treatment of gabapentin on α2δ-1 also significantly reduced the occurrence of apoptosis. KO of Cacna2d1 also reduced the ICH-induced levels of inflammatory factors. Furthermore, neural functions were also significantly improved.
conclusionCacna2d1 KO alleviates cerebral hematoma in ICH mice, exhibits a significant regulating effect on its secondary injuries such as neuronal apoptosis and inflammation, and restores the nerve functions of ICH mice. Loss of Cacna2d1 can provide useful therapeutic clues for ICH treatment.
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