ArticleJournal of molecular neuroscience : MN2012
Changes in lipid-sensitive two-pore domain potassium channel TREK-1 expression and its involvement in astrogliosis following cerebral ischemia in rats.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- TREK-1 in central nervous system diseases.Chinese medical journal · 2026Article
- TREK-1 and epilepsy: regulating the balance of KBehavioral and brain functions : BBF · 2025Review
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- Behavioural and biochemical indications of the antidepressant activities of essential oils fromIBRO neuroscience reports · 2021Article
- Intracellular activation of full-length human TREK-1 channel by hypoxia, high lactate, and low pH denotes polymodal integration by ischemic factors.Pflugers Archiv : European journal of physiology · 2021Article
- Contribution of Neuronal and Glial Two-Pore-Domain Potassium Channels in Health and Neurological Disorders.Neural plasticity · 2021Review
- The Efficacy of N-Butylphthalide and Dexamethasone Combined with Hyperbaric Oxygen on Delayed Encephalopathy After Acute Carbon Monoxide Poisoning.Drug design, development and therapy · 2020Article
- The Lectin LecA Sensitizes the Human Stretch-Activated Channel TREK-1 but Not Piezo1 and Binds Selectively to Cardiac Non-myocytes.Frontiers in physiology · 2020Article
- Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells.Frontiers in cellular neuroscience · 2020Article
- Role of TREK-1 in Health and Disease, Focus on the Central Nervous System.Frontiers in pharmacology · 2019Review
- A-Kinase-Anchoring Protein (AKAP150) is expressed in Astrocytes and Upregulated in Response to Ischemia.Neuroscience · 2018Article
- Two-pore Domain Potassium Channels in Astrocytes.Experimental neurobiology · 2016Review
- Over-expressed human TREK-1 inhibits CHO cell proliferation via inhibiting PKA and p38 MAPK pathways and subsequently inducing G1 arrest.Acta pharmacologica Sinica · 2016Article
- Lactate modulates the intracellular pH sensitivity of human TREK1 channels.Pflugers Archiv : European journal of physiology · 2016Article
- A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives.BioMed research international · 2016Review
- Ischaemic concentrations of lactate increase TREK1 channel activity by interacting with a single histidine residue in the carboxy terminal domain.The Journal of physiology · 2016Article
- The Role of the Two-Pore Domain Potassium Channel TREK-1 in the Therapeutic Effects of Escitalopram in a Rat Model of Poststroke Depression.CNS neuroscience & therapeutics · 2015Article
- The CNS under pathophysiologic attack--examining the role of K₂p channels.Pflugers Archiv : European journal of physiology · 2015Review
- Electrophysiology and pharmacology of tandem domain potassium channel TREK-1 related BDNF synthesis in rat astrocytes.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- The inhibitor of volume-regulated anion channels DCPIB activates TREK potassium channels in cultured astrocytes.British journal of pharmacology · 2013Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes play an active and important role in the pathophysiology of cerebral ischemia. We have previously shown that mature hipppocampal astrocytes functionally express two-pore domain K(+) channel TREK-1, which significantly contributes to the passive conductance and help to set the negative resting membrane potential essential for the optimal operation of some astrocytic homeostatic functions. However, its expression under ischemic conditions remains to be determined. In this study, we examined the expression of TREK-1 in rat brain under physiological and focal ischemia conditions. The results show that TREK-1 was broadly expressed on astrocytes and neurons in the cortex, CA1 region of hippocampus. After middle cerebral artery occlusion induced focal ischemia, the TREK-1 expression was significantly increased at days 3, 7 and 30 following reperfusion, which correlated with reactive astrogliosis in the cortex and hippocampus. Cultured cortical astrocytes also express TREK-1. TREK-1 inhibitor quinine inhibited the proliferation of astrocytes exposed to hypoxia condition. These data provide evidence showing the astrocytic TREK-1 involvement in ischemia pathology.
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