Increasing evidence is pointing to a central role for astrocytes in ALS disease pathology (see stories from October 2011 and February 2014). A new study led by Michael Sofroniew and Baljit Khakh at the University of California, Los Angeles and published on March 30th in Nature Neuroscience, implicates astrocytes yet again, this time in the context of Huntington’s disease (HD). The investigators examined the role of striatal astrocytes in two distinct mouse models of HD and found that in both, astrocytes expressing mutant huntingtin lack a specific potassium channel, Kir4.1, which is crucial for cleaning up extracellular potassium. The resulting increase in extracellular potassium leads to hyperexcitability of striatal neurons, and increasing Kir4.1 expression in a mouse model of HD partially alleviates the motor deficits characteristic of the disease. Interestingly, a role for impaired potassium channel function in ALS has also been recently described (see this newsletter). Click here to read more.
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