ArticleJournal of neuropathology and experimental neurology2012
Loss of perivascular Kir4.1 potassium channels in the sclerotic hippocampus of patients with mesial temporal lobe epilepsy.
Article in Journal of neuropathology and experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Mechanisms Underlying Aquaporin-4 Subcellular Mislocalization in Epilepsy.Frontiers in cellular neuroscience · 2022Pooled it
- A stage-resolved neuron-glia transcriptional atlas reveals a glial inflammatory pivot in epilepsy.Acta neuropathologica communications · 2026Article
- Nonlinear dynamics of seizure suppression via optogenetic modulation of neuron-astrocyte interaction.Scientific reports · 2026Article
- The spatial architecture of neuroimmune interactions in epilepsy.Frontiers in immunology · 2026Review
- The Role of Blood-Brain Barrier Disruption in Epilepsy: Mechanisms and Consequences.Neurology international · 2025Review
- WONOEP XVII appraisal: Targeting network excitability beyond the synapse -Neurotransmitter, ionic, and electro -diffusions.Epilepsia · 2025Review
- Organophosphate Chemical Nerve Agents, Oxidative Stress, and NADPH Oxidase Inhibitors: An Overview.International journal of molecular sciences · 2025Review
- Epileptic seizure biophysics: the role of local voltage difference.Military Medical Research · 2025Article
- Small molecule ion channel agonist/antagonist screen reveals seizure suppression via glial Irk2 activation in a Drosophila model of Dup15q syndrome.Neurobiology of disease · 2025Article
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- Changes in the excitability of the medial parabrachial nucleus neurons during the chronic phase of pilocarpine-induced epilepsy in mice.Frontiers in pharmacology · 2025Article
- Astrocytes as critical players of the fine balance between inhibition and excitation in the brain: spreading depolarization as a mechanism to curb epileptic activity.Frontiers in network physiology · 2024Review
- Astrocytic pathology in Alpers' syndrome.Acta neuropathologica communications · 2023Article
- Overview Article Astrocytes as Initiators of Epilepsy.Neurochemical research · 2023Review
- Glioma epileptiform activity and progression are driven by IGSF3-mediated potassium dysregulation.Neuron · 2023Article
- Astrocyte reactivity in a mouse model of SCN8A epileptic encephalopathy.Epilepsia open · 2022Article
- Perspectives on the basis of seizure-induced respiratory dysfunction.Frontiers in neural circuits · 2022Review
- Cellular changes at the glia-neuro-vascular interface in definite idiopathic normal pressure hydrocephalus.Frontiers in cellular neuroscience · 2022Article
- A New Perspective on the Pathophysiology of Idiopathic Intracranial Hypertension: Role of the Glia-Neuro-Vascular Interface.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent experimental data in mice have shown that the inwardly rectifying K channel Kir4.1 mediates K spatial buffering in the hippocampus. Here we used immunohistochemistry to examine the distribution of Kir4.1 in hippocampi from patients with medication-refractory temporal lobe epilepsy. The selectivity of the antibody was confirmed in mice with a glial conditional deletion of the gene encoding Kir4.1. These mice showed a complete loss of labeled cells, indicating that Kir4.1 is restricted to glia. In human cases, Kir4.1 immunoreactivity observed in cells morphologically consistent with astrocytes was significantly reduced in 12 patients with hippocampal sclerosis versus 11 patients without sclerosis and 4 normal autopsy controls. Loss of astrocytic Kir4.1 immunoreactivity was most pronounced around vessels and was restricted to gliotic areas. Loss of Kir4.1 expression was associated with loss of dystrophin and α-syntrophin, but not with loss of β-dystroglycan, suggesting partial disruption of the dystrophin-associated protein complex. The changes identified in patients with hippocampal sclerosis likely interfere with K homeostasis and may contribute to the epileptogenicity of the sclerotic hippocampus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.