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HAP1 interacts with 14-3-3 to regulate epileptic seizure via GABAAR-mediated inhibitory synaptic transmission in pentylenetetrazole rat model.

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机构： [1]Department of Neurosurgery, Chongqing University Jiangjin Hospital, School of Medicine, Chongqing University, Chongqing, China [2]Department of Endoscopy center, Chongqing Jiangjin District Hospital of Traditional Chinese Medicine, Chongqing, China [3]Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China [4]Department of Neurology, The First People’s Hospital of Yunnan Province/The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China

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Disruption of γ-aminobutyric acid type A receptors (GABAARs) synaptic clustering and a decrease number in the plasma membrane are thought to contribute to the alteration in the balance between excitatory and inhibitory neurotransmission in the epilepsy. Thus, it is important to elucidate the molecular mechanisms that regulate the stabilities of surface GABAARs populations as well as their concentrations at inhibitory synapses. However, the mechanism that delivers GABAARs to plasma membrane has not been conclusively determined. Our previous research indicated that huntingtin-associated protein 1 (HAP1), a major facilitator of pathological variations in membrane trafficking, modulates epileptic seizure by regulating GABAARs-mediated inhibitory synaptic transmission in pentylenetetrazole (PTZ)-induced epileptic rats. However, a detailed molecular interaction networks comprising GABAARs and HAP1 is necessary for studying and investigating new treatment targets for epilepsy. In this study, we indicate that HAP1 specifically interacts with 14-3-3, a protein that functions as a chaperone, forming a cargo adaptor complex to regulate surface GABAARs expression and the inhibitory post-synaptic current amplitudes. Disrupting the HAP1/14-3-3 complex decreases the strength of GABAARs-mediated inhibitory synaptic transmission in epilepsy. Taken together, HAP1/14-3-3 complex is linked to inhibitory synaptic transmission in evoking seizures, therefore, it is a possible drug target for epilepsy.Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.

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出版当年[2022]版：

大类 | 4 区医学

小类 | 4 区神经科学

最新[2023]版：

大类 | 4 区医学

小类 | 4 区神经科学

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Q3 NEUROSCIENCES

最新[2023]版：

Q3 NEUROSCIENCES

影响因子： 2.4 最新[2023版] 2.6 最新五年平均 2.904 出版当年[2021版] 2.892 出版当年五年平均 3.322 出版前一年[2020版] 2.9 出版后一年[2022版]

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第一作者机构： [1]Department of Neurosurgery, Chongqing University Jiangjin Hospital, School of Medicine, Chongqing University, Chongqing, China

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通讯作者：

通讯机构： [4]Department of Neurology, The First People’s Hospital of Yunnan Province/The Affiliated Hospital of Kunming University of Science and Technology, Kunming, Yunnan, China [*1]Department of Neurology, The First People’s Hospital of Yunnan Province/The Affiliated Hospital of Kunming University of Science and Technology, No. 157, Jinbi Road, Xishan District, 650034 Kunming, Yunnan, China.

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