Back to search

Article

The paradoxical effects of K <sup>+</sup> channel gain-of-function are mediated by GABAergic neuron hypoexcitability and hyperconnectivity

2020-03-06

Abstract excerpt

<h4>SUMMARY</h4> Gain-of-function (GOF) variants in K + channels cause severe childhood epilepsies, but there are no mechanisms to explain how increased K + currents lead to network hyperexcitability. Here, we introduced a human Na + -activated K + (K Na ) channel variant ( KCNT1-Y796H ) into mice and, using a multiplatform approach, found motor cortex hyperexcitability and early-onset seizures, phenotypes...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
4b68c1ff-c86b-5e8b-81ff-cccb9c2283b6
DOI
10.1101/2020.03.05.978841
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
The paradoxical effects of K <sup>+</sup> channel gain-of-function are mediated by GABAergic neuron hypoexcitability and hyperconnectivityDOI 10.1101/2020.03.05.978841
Disease-causing Slack potassium channel mutations produce opposite effects on excitability of excitatory and inhibitory neuronsSemantic proximity
Heterozygous expression of a <i>Kcnt1</i> gain-of-function variant has differential effects on SST- and PV-expressing cortical GABAergic neuronsSemantic proximity
Severe deficiency of voltage-gated sodium channel Na <sub>V</sub> 1.2 elevates neuronal excitability in adult miceSemantic proximity
Novel Gain of Function Mouse Model of KCNT1-Related EpilepsySemantic proximity
Potassium Channel Gain of Function in Epilepsy: An Unresolved ParadoxSemantic proximity
<i>KCNH1</i> variants associated with neurodevelopmental disorders exhibit prominent gain-of-functionSemantic proximity
Biophysical characterization and modeling of <i>SCN1A</i> gain-of-function predicts interneuron hyperexcitability and a predisposition to network instability through homeostatic plasticitySemantic proximity
Disease-causing Slack potassium channel mutations produce opposite effects on excitability of excitatory and inhibitory neurons.Semantic proximity
Inherited neuronal ion channelopathies: new windows on complex neurological diseases.Semantic proximity
Impaired excitability of fast-spiking neurons in a novel mouse model of <i>KCNC1</i> epileptic encephalopathySemantic proximity
Context-dependent NMDA receptor dysfunction predicts seizure treatment in mice with human GluN1 variantSemantic proximity
<i>SCN1A</i> -deficient hiPSC-derived excitatory neuronal networks display mutation-specific phenotypesSemantic proximity
Select a neighboring publication to make it the new centre.