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In Huntington’s disease (HD) – a devastating autosomal-dominant neurodegenerative disease – the striatum displays reduced cholinergic markers, despite the resiliency of cholinergic interneurons (ChIs) – the source of striatal acetylcholine – to the neurodegeneration that decimates striatal projection neurons. Autonomous spiking of ChIs is unchanged in transgenic HD mice, suggesting a functional deficit in extrinsically driven activity. Using two transgenic mouse models of HD, we show that ChI responses to cortical input are boosted by a post-synaptic up-regulation of the persistent sodium current. This boosting is replicated by in wild-type mice by diminished activation of group I metabotropic glutamate receptors (mGluRs). Activation of group I mGluRs in HD mice counters the boosting. We propose that the recently described loss of thalamic synapses in striatum, reduces group I mGluR activation in ChIs which promotes boosting of cortical inputs. The augmentation of cortical inputs may function to compensate for the lost thalamic glutamatergic drive.