ArticleMetabolic brain disease2019
Excessive corticosterone induces excitotoxicity of hippocampal neurons and sensitivity of potassium channels via insulin-signaling pathway.
Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Pharmacological targeting of cognitive impairment in depression: recent developments and challenges in human clinical research.Translational psychiatry · 2022Review
- TPEN attenuates amyloid-βMolecular brain · 2021Article
- Potential role of insulin on the pathogenesis of depression.Cell proliferation · 2020Review
- Xiaoyao Kangai Jieyu Fang, a Chinese Herbal Formulation, Ameliorates Cancer-Related Depression Concurrent with Breast Cancer in Mice via Promoting Hippocampal Synaptic Plasticity.Evidence-based complementary and alternative medicine : eCAM · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Corticosterone (CORT) is a kind of corticosteroid produced by cortex of adrenal glands. Hypothalamic-pituitary-adrenal (HPA) axis hyperfunction leads to excessive CORT, which is associated with depression. Few studies have investigated the role of CORT in voltage-gated ion channels and its upstream signaling pathway in central nervous system. In this study, we investigated the mechanism of excessive CORT resulting in brain impairment on voltage-gated ion channels, and its upstream signaling effectors in hippocampal CA1 neurons. The action potential (AP) and voltage-gated potassium currents were determined by using whole-cell patch-clamp. Insulin and CORT improved the neuronal excitability. Independent effects existed in transient potassium channel (I
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