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Scientists reveal the inherent plasticity of neurons and its pathological significance in epileptic seizures

 Last Update: 2021-09-03
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Scientists reveal the inherent plasticity of neurons and its pathological significance in epileptic seizures

Scientists reveal the inherent plasticity of neurons and their pathological significance in epileptic seizures Scientists reveal the inherent plasticity of neurons and their pathological significance in epileptic seizures

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At 23:00, July 20, 2021, Beijing time, Cell Reports published an online paper entitled "TRESK channel contributes to depolarization-induced shunting inhibition and modulates epileptic seizures"
.

Cell Reports

The study revealed a phenomenon of intrinsic short-term plasticity of neurons and its molecular mechanism, and revealed that this phenomenon has important pathological significance in the process of epilepsy
.

Professor Chen Rongqing from Southern Medical University and Professor Werner Kilb from the University of Mainz, Germany are the co-corresponding authors of the paper.

First of all, the paper found that the function of pyramidal neurons in the hippocampus was inhibited after seizure-like continuous depolarization, that is, motor electrical production obstacles and ion channel receptors (including gamma-aminobutyric acid receptors, glutamate receptors).
The decrease in the reactivity of the receptor and glycine receptor is due to the membrane shunt inhibitory effect formed by the continuous depolarization induced by the increase of cell membrane conductivity
.

Researchers call this phenomenon "Depolarization-induced shunting inhibition (DShI)"

Secondly, through pharmacology and gene knockout experiments, the paper discovered the molecular mechanism of DShI induction: continuous depolarization triggers the increase of intracellular calcium ion concentration, calcium ion activates calcineurin, which enhances potassium ion channels belonging to the tandem pore domain The opening of the TRESK channel of the family, and the activation of the TRESK channel mediates DShI through the membrane shunt inhibitory effect
.

Finally, the paper found that gene knockout of the TRESK channel delayed the termination of epileptic seizures in experimental mice and shortened the suppression time after seizures, thereby increasing the severity of epilepsy
.

For example, knockout mice of the TRESK channel are more likely to have higher-grade seizures, and more likely to have status epilepticus and death caused by epilepsy