Potassium channel dysfunction in neurons and astrocytes in Huntington's disease
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Potassium channel dysfunction in neurons and astrocytes in Huntington's disease. / Zhang, Xiao; Wan, Jie-Qing; Tong, Xiao-Ping.
In: CNS Neuroscience and Therapeutics, Vol. 24, No. 4, 2018, p. 311-318.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Potassium channel dysfunction in neurons and astrocytes in Huntington's disease
AU - Zhang, Xiao
AU - Wan, Jie-Qing
AU - Tong, Xiao-Ping
N1 - © 2018 John Wiley & Sons Ltd.
PY - 2018
Y1 - 2018
N2 - Huntington's disease (HD) is a late-onset fatal neurodegenerative disease, characterized by progressive movement disorders, psychiatric symptoms, and cognitive impairment. The cytosine-adenine-guanine (CAG) triplet expansion encoding glutamine present in the protein huntingtin (Htt), produces widespread neuronal and glial pathology. Mutant huntingtin (mHtt) nuclear aggregates are the primary cause of cortical and striatal neuron degeneration, neuronal inflammation, apoptosis and eventual cell loss. The precise mechanisms underlying the pathogenesis of neurodegeneration in HD remain poorly understood and HD patients have no current cure. Potassium channels are widely expressed in most cell types. In neurons, they play a crucial role in setting the resting membrane potential, mediating the rapid repolarization phase of the action potential and controlling sub-threshold oscillations of membrane potentials. In glial cells, their major contributions are maintaining the resting membrane potential and buffering extracellular K+ . Thus, potassium channels have an essential function in both physiological and pathological brain conditions. This review summarizes recent progress on potassium channels involved in the pathology of HD by using different HD mouse models. Exploring the dysfunction of potassium channels in the brain illustrates new approaches for targeting this channel for the treatment of HD.
AB - Huntington's disease (HD) is a late-onset fatal neurodegenerative disease, characterized by progressive movement disorders, psychiatric symptoms, and cognitive impairment. The cytosine-adenine-guanine (CAG) triplet expansion encoding glutamine present in the protein huntingtin (Htt), produces widespread neuronal and glial pathology. Mutant huntingtin (mHtt) nuclear aggregates are the primary cause of cortical and striatal neuron degeneration, neuronal inflammation, apoptosis and eventual cell loss. The precise mechanisms underlying the pathogenesis of neurodegeneration in HD remain poorly understood and HD patients have no current cure. Potassium channels are widely expressed in most cell types. In neurons, they play a crucial role in setting the resting membrane potential, mediating the rapid repolarization phase of the action potential and controlling sub-threshold oscillations of membrane potentials. In glial cells, their major contributions are maintaining the resting membrane potential and buffering extracellular K+ . Thus, potassium channels have an essential function in both physiological and pathological brain conditions. This review summarizes recent progress on potassium channels involved in the pathology of HD by using different HD mouse models. Exploring the dysfunction of potassium channels in the brain illustrates new approaches for targeting this channel for the treatment of HD.
KW - Animals
KW - Astrocytes/metabolism
KW - Humans
KW - Huntington Disease/metabolism
KW - Neurons/metabolism
KW - Potassium Channels/metabolism
U2 - 10.1111/cns.12804
DO - 10.1111/cns.12804
M3 - Review
C2 - 29377621
VL - 24
SP - 311
EP - 318
JO - CNS Neuroscience and Therapeutics
JF - CNS Neuroscience and Therapeutics
SN - 1755-5930
IS - 4
ER -
ID: 324308190