ArticleNeurobiology of disease2013
Loss of the Kv1.1 potassium channel promotes pathologic sharp waves and high frequency oscillations in in vitro hippocampal slices.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 72 citations in OpenAlex.
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- Targeted Reduction of Excessive Mitochondrial Superoxide by Mitoquinone Rescues Cognitive Impairment Without Affecting Spontaneous Recurrent Seizures in a Mouse Model of Temporal Lobe Epilepsy.Antioxidants (Basel, Switzerland) · 2026Article
- Temporal lobe epilepsy is associated with neuroinflammation, extracellular matrix remodeling, and synaptic protein alterations.Frontiers in molecular neuroscience · 2026Article
- Properties of Heterochannels Kv(1.1-1.2)International journal of molecular sciences · 2025Article
- Serotonin Modulation of Dorsoventral Hippocampus in Physiology and Schizophrenia.International journal of molecular sciences · 2025Review
- Compensatory Regulation of Excitation/Inhibition Balance in the Ventral Hippocampus: Insights from Fragile X Syndrome.Biology · 2025Review
- Seizures and premature death in mice with targeted Kv1.1 deficiency in corticolimbic circuits.Brain communications · 2025Article
- Opposite serotonergic modulation of sharp waves in the dorsal and ventral hippocampus.Frontiers in synaptic neuroscience · 2025Article
- Altered ventilatory responses to hypercapnia-hypoxia challenges in a preclinical SUDEP model involve orexin neurons.Neurobiology of disease · 2024Article
- Orexin receptors regulate hippocampal sharp wave-ripple complexes in ex vivo slices.European journal of pharmacology · 2023Article
- Rescue of sharp wave-ripples and prevention of network hyperexcitability in the ventral but not the dorsal hippocampus of a rat model of fragile X syndrome.Frontiers in cellular neuroscience · 2023Article
- Identification of key potassium channel genes of temporal lobe epilepsy by bioinformatics analyses and experimental verification.Frontiers in neurology · 2023Article
- Ascorbic Acid Reduces Neurotransmission, Synaptic Plasticity, and Spontaneous Hippocampal Rhythms in In Vitro Slices.Nutrients · 2022Article
- A review on 3D printing functional brain model.Biomicrofluidics · 2022Review
- Pharmacoresponsiveness of spontaneous recurrent seizures and the comorbid sleep disorder of epileptic Kcna1-null mice.European journal of pharmacology · 2021Article
- Three dimensional microelectrodes enable high signal and spatial resolution for neural seizure recordings in brain slices and freely behaving animals.Scientific reports · 2021Article
- KScientific reports · 2021Article
- Carbamazepine Reduces Sharp Wave-Ripple Complexes and Exerts Synapse-Specific Inhibition of Neurotransmission in Ex Vivo Hippocampal Slices.Brain sciences · 2021Article
- Chronic Ethanol Exposures Leads to a Negative Affective State in Female Rats That Is Accompanied by a Paradoxical Decrease in Ventral Hippocampus Excitability.Frontiers in neuroscience · 2021Article
- Kv1.1 Channelopathies: Pathophysiological Mechanisms and Therapeutic Approaches.International journal of molecular sciences · 2020Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
In human disease, channelopathies involving functional reduction of the delayed rectifier potassium channel α-subunit Kv1.1 - either by mutation or autoimmune inhibition - result in temporal lobe epilepsy. Kv1.1 is prominently expressed in the axons of the hippocampal tri-synaptic pathway, suggesting its absence will result in widespread effects on normal network oscillatory activity. Here, we performed in vitro extracellular recordings using a multielectrode array to determine the effects of loss of Kv1.1 on spontaneous sharp waves (SPWs) and high frequency oscillations (HFOs). We found that Kcna1-null hippocampi generate SPWs and ripples (80-200Hz bandwidth) with a 50% increased rate of incidence and 50% longer duration, and that epilepsy-associated pathologic HFOs in the fast ripple bandwidth (200-600Hz) are also present. Furthermore, Kcna1-null CA3 has enhanced coupling of excitatory inputs and population spike generation and CA3 principal cells have reduced spike timing reliability. Removing the influence of mossy fiber and perforant path inputs by micro-dissecting the Kcna1-null CA3 region mostly rescued the oscillatory behavior and improved spike timing. We found that Kcna1-null mossy fibers and medial perforant path axons are hyperexcitable and produce greater pre- and post-synaptic responses with reduced paired-pulse ratios suggesting increased neurotransmitter release at these terminals. These findings were recapitulated in wild-type slices exposed to the Kv1.1 inhibitor dendrotoxin-κ. Collectively, these data indicate that loss of Kv1.1 enhances synaptic release in the CA3 region, which reduces spike timing precision of individual neurons leading to disorganization of network oscillatory activity and promotes the emergence of fast ripples.
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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.