Astrocyte Kir4.1 ion channel deficits contribute to neuronal dysfunction in Huntington's disease model mice

In this study, the authors show that altered medium spiny neuron excitability and symptom onset in Huntington's disease model mice is associated with decreased expression of Kir4.1 and impaired K+ handling by astrocytes. Exogenous expression of Kir4.1 could partially rescue motor function and prolong survival in HD mice.