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February 5, 2021eLife51 citationsOpen Access

Dyshomeostatic modulation of Ca2+-activated K+ channels in a human neuronal model of KCNQ2 encephalopathy

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Population

Human induced pluripotent stem cell (iPSC)-derived excitatory neurons modeling KCNQ2 encephalopathy

Comparison

Gene editing to establish a disease model and… vs Control neurons

Design

Preclinical

Key result

Patient iPSC-derived neurons with the KCNQ2 R581Q mutation exhibited progressive escalation of burst firing, faster action potential repolarization, and larger post-burst afterhyperpolarization compared to isogenic controls.

Authors

DSDina SimkinKMKelly A. MarshallCVCarlos G. Vanoye

Discussion

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Overview

iPSC neuron phenotypes suggest compensatory K+ channel changes in KCNQ2 disorders; leaves open translation to in vivo mechanisms or therapies.

Structured PICO

P
Population
iPSC-derived cortical excitatory neurons from a 13-year-old female with KCNQ2-DEE and isogenic controls, studied in vitro over 5 weeks.
E
Exposure
Gene editing to establish a disease model and chronic inhibition of M-current
C
Comparator
Control neurons
O
Outcome
Functional electrophysiological properties of differentiated excitatory neuronssurrogate

Dyshomeostatic mechanisms compound KCNQ2 loss-of-function, altering the neurodevelopmental trajectory and electrophysiological properties of patient iPSC-derived neurons.

Main Result

p-value: p=<0.0001

Limitations

  • The model system is exclusively comprised of glutamatergic excitatory neurons, lacking inhibitory interneurons.

Cite This Study

Simkin et al. (2021) studied KCNQ2 epileptic encephalopathy (n=4). KCNQ2 R581Q mutation vs. Isogenic mutation-corrected control neurons was evaluated on Spontaneous neuronal activity and burst firing (p=<0.0001). Patient iPSC-derived neurons with the KCNQ2 R581Q mutation exhibited progressive escalation of burst firing, faster action potential repolarization, and larger post-burst afterhyperpolarization compared to isogenic controls.

synapsesocial.com/papers/6a991a4160c7aa7f93273421https://doi.org/10.7554/elife.64434
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