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TRESK channel contributes to depolarization-induced shunting
AAV-Tresk was used for gene over-expression. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Custom-Made AAV  rAAV2/9-Ef1α-Tresk-eYFP-WPRE-pA
Control  PT-0098 rAAV2/9-Ef1α-eYFP-WPRE-pA
Weiyuan Huang, Yue Ke, Jianping Zhu, Shuai Liu, Jin Cong, Hailin Ye, Yanwu Guo, Kewan Wang, Zhenhai Zhang, Wenxiang Meng, Tian-Ming Gao, Heiko J Luhmann, Werner Kilb, Rongqing Chen
Pub Date: 2021-07-21, DOI: 10.1016/j.celrep.2021.109404, Email: [email protected]
Glutamatergic and GABAergic synaptic transmission controls excitation and inhibition of postsynaptic neurons, whereas activity of ion channels modulates neuronal intrinsic excitability. However, it is unclear how excessive neuronal excitation affects intrinsic inhibition to regain homeostatic stability under physiological or pathophysiological conditions. Here, we report that a seizure-like sustained depolarization can induce short-term inhibition of hippocampal CA3 neurons via a mechanism of membrane shunting. This depolarization-induced shunting inhibition (DShI) mediates a non-synaptic, but neuronal intrinsic, short-term plasticity that is able to suppress action potential generation and postsynaptic responses by activated ionotropic receptors. We demonstrate that the TRESK channel significantly contributes to DShI. Disruption of DShI by genetic knockout of TRESK exacerbates the sensitivity and severity of epileptic seizures of mice, whereas overexpression of TRESK attenuates seizures. In summary, these results uncover a type of homeostatic intrinsic plasticity and its underlying mechanism. TRESK might represent a therapeutic target for antiepileptic drugs.
In this study, the authors find sustained depolarization-induced shunting inhibition (DShI) which is induced by seizure-like and seizure-mimicking sustained depolarizations. The inhibitory action and time course of DShI is sufficient to explain the termination of ictal epileptiform activity and postictal depression. TRESK contributes to DShI and modulates seizures.
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