ArticleCurrent neurovascular research2022
Chronic Cerebral Hypoperfusion-induced Dysregulations of Hyperpolarization- activated Cyclic Nucleotide-gated, KCNQ and G Protein-coupled Inwardly Rectifying Potassium Channels Correlated with Susceptibility and Unsusceptibility to Anxiety Behaviors.
Article in Current neurovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- ZD7288 ameliorates long-term cerebral ischemia reperfusion-induced deterioration of spatial memory by regulating the expressions of NMDA receptor subunits in rats.Scientific reports · 2025Article
- Downregulation of the HCN1 Channel Alleviates Anxiety- and Depression-Like Behaviors in Mice With Cerebral Ischemia-Reperfusion Injury by Suppressing the NLRP3 Inflammasome.Journal of the American Heart Association · 2025Article
- Review
- Behavioral and neuro-functional consequences of eliminating the KCNQ3 GABA binding site in mice.Frontiers in molecular neuroscience · 2023Article
- Regulatory Molecules of Synaptic Plasticity in Anxiety Disorder.International journal of general medicine · 2023Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCerebrovascular lesions could induce affective disorders; however, the depression- and anxiety-related symptoms caused by Chronic Cerebral Hypoperfusion (CCH) and the roles of different Hyperpolarization-activated Cyclic Nucleotide-gated (HCN), KCNQ and G protein-coupled inwardly rectifying potassium (GirK) channel subunits in these pathological processes have been poorly elucidated so far.
objectiveTo investigate the behavioral change and the alteration of HCN, KCNQ, and GirK subunits in amygdale rats suffering from CCH.
methodsPermanent bilateral occlusion of the common carotid arteries was used to induce CCH. Anxiety and depression levels were assessed by the elevated plus maze test, sucrose preference test and forced swimming test to classify rats as highly anxious or depressive 'susceptibility' vs. 'unsusceptibility'. The expression of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrKB), HCN1/2, KCNQ2/3, and GirK1/2/3 were quantified by Western blotting.
resultsThe main emotional change caused by 4 weeks of CCH is likely to be anxiety-like behavior (50%), accompanied by a down-regulation of BDNF and TrKB expression in amygdale. The increase of HCN1 and decrease of KCNQ3 expression in amygdale may be factors to blame for anxiety- like symptom caused by CCH, and the increase of KCNQ2 and Girk1 expression in amygdale may play a role in resilience to the anxiety induced by CCH.
conclusionThe different subunits of HCN, KCNQ and GirK channels in amygdale may contribute to distinct response to aversive stimuli or stress induced by CCH that evokes divergent influences on anxiety-like behavior in rats.
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