ArticleCNS neuroscience & therapeutics2019
The absence of NIPA2 enhances neural excitability through BK (big potassium) channels.
Article in CNS neuroscience & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Mechanistic studies of the human NIPA2 transporter.Nature communications · 2026Article
- Article
- Transcriptome Profiling of Hippocampus After Cerebral Hypoperfusion in Mice.Journal of molecular neuroscience : MN · 2023Article
- Prader-Willi syndrome, deletion subtypes, and magnesium: Potential impact on clinical findings.American journal of medical genetics. Part A · 2022Article
- Hypothalamic neuropeptides and neurocircuitries in Prader Willi syndrome.Journal of neuroendocrinology · 2021Review
- The abnormal firing of Purkinje cells in the knockin mouse model of DYT1 dystonia.Brain research bulletin · 2020Article
- General Aspects of Metal Ions as Signaling Agents in Health and Disease.Biomolecules · 2020Review
- The absence of NIPA2 enhances neural excitability through BK (big potassium) channels.CNS neuroscience & therapeutics · 2019Article
- Magnesium Supplement and the 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome: A Potential Treatment?International journal of molecular sciences · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo reveal the pathogenesis and find the precision treatment for the childhood absence epilepsy (CAE) patients with NIPA2 mutations.
methodsWe performed whole-cell patch-clamp recordings to measure the electrophysiological properties of layer V neocortical somatosensory pyramidal neurons in wild-type (WT) and NIPA2-knockout mice.
resultsWe identified that layer V neocortical somatosensory pyramidal neurons isolated from the NIPA2-knockout mice displayed higher frequency of spontaneous and evoked action potential, broader half-width of evoked action potential, and smaller currents of BK channels than those from the WT mice. NS11021, a specific BK channel opener, reduced neuronal excitability in the NIPA2-knockout mice. Paxilline, a selective BK channel blocker, treated WT neurons and could simulate the situation of NIPA2-knockout group, thereby suggesting that the absence of NIPA2 enhanced the excitability of neocortical somatosensory pyramidal neurons by decreasing the currents of BK channels. Zonisamide, an anti-epilepsy drug, reduced action potential firing in NIPA2-knockout mice through increasing BK channel currents.
conclusionThe results indicate that the absence of NIPA2 enhances neural excitability through BK channels. Zonisamide is probably a potential treatment for NIPA2 mutation-induced epilepsy, which may provide a basis for the development of new treatment strategies for epilepsy.
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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.