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The adjustment of γ-aminobutyric acidA tonic subunits in Huntington's disease:from transcription to translation to synaptic levels into the neostriatum

摘要:

γ-Aminobutyric acid (GABA), plays a key role in all stages of life, also is considered the main inhibitory neurotransmitter. GABA activates two kind of membrane receptors known as GABAAand GABAB, the first one is responsible to render tonic inhibition by pentameric receptors containing α4?6, β3, δ, or ρ1?3 sub-units, they are located at perisynaptic and/or in extrasynaptic regions. The biophysical properties of GABAA tonic inhibition have been related with cellular protection against excitotoxic injury and cell death in pres-ence of excessive excitation. On this basis, GABAAtonic inhibition has been proposed as a potential target for therapeutic intervention of Huntington's disease. Huntington's disease is a neurodegenerative disorder caused by a genetic mutation of the huntingtin protein. For experimental studies of Huntington's disease mouse models have been developed, such as R6/1, R6/2, HdhQ92, HdhQ150, as well as YAC128. In all of them, some key experimental reports are focused on neostriatum. The neostriatum is considered as the most important connection between cerebral cortex and basal ganglia structures, its cytology display two pathways called direct and indirect constituted by medium sized spiny neurons expressing dopamine D1 and D2 receptors respectively, they display strong expression of many types of GABAAreceptors, including tonic subunits. The studies about of GABAAtonic subunits and Huntington's disease into the neostriatum are rising in recent years, suggesting interesting changes in their expression and localization which can be used as a strategy to delay the cellular damage caused by the imbalance between excitation and inhibition, a hallmark of Huntington's disease.

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作者单位: Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile;Center for Interdisciplinary Studies on the Nervous System (CISNe), Universidad Austral de Chile, Valdivia, Chile;Departamento de Fisiología, Biofísica y Neurociencias, Cinvestav del IPN, Ciudad de México, México [1] Queensland Brain Institute, The University of Queensland, Brisbane, Australia [2] Laboratorio de Neurociencias, Departamento de Biología, Facultad de Química y Biología, Universidad de Santiago de Chile, Santiago de Chile, Chile [3] Departamento de Fisiología, Biofísica y Neurociencias, Cinvestav del IPN, Ciudad de México, México [4] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile;Center for Interdisciplinary Studies on the Nervous System (CISNe), Universidad Austral de Chile, Valdivia, Chile [5]
期刊: 《中国神经再生研究(英文版)》2018年13卷4期 584-590页 SCIMEDLINEISTICCSCDBP
栏目名称: INVITED REVIEWS
DOI: 10.4103/1673-5374.230270
发布时间: 2018-05-31
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