Huntington’s disease (HD) is a progressive neurodegenerative disorder with no cure, characterized by significant neurodegeneration of striatal GABAergic medium spiny neurons (MSNs). Early stages of the disease are characterized by the loss of dopamine 2 receptor-expressing MSNs (D2 MSNs) followed by degeneration of dopamine 1 receptor-expressing MSNs (D1 MSNs), leading to aberrant basal ganglia signaling. While the early degeneration of D2 MSNs and impaired GABAergic transmission are well-documented, potassium chloride cotransporter 2 (KCC2), a key regulator of GABAergic signaling, has not been characterized in D1 and D2 MSNs in HD. We aimed to investigate whether KCC2 function was differentially altered in D1 and D2 MSNs and may contribute to the early degeneration of D2 MSNs in symptomatic R6/2 mice. We used electrophysiology to record the reversal potential for GABAA receptors (EGABA), a read-out for KCC2 function, in striatal D1 and D2 MSNs and their corresponding output structures. During the early symptomatic phase (P55-P65), KCC2 function was reduced in D2 MSNs in R6/2 mice, with no apparent change in D1 MSNs. KCC2 was also downregulated in the globus pallidus externa, resulting in GABA-mediated excitation. When we overexpressed KCC2 using AAV-mediated delivery of this transporter to D2 MSNs, we delayed the onset of motor impairments in R6/2 mice. We demonstrate that KCC2 is differentially altered in D1 and D2 MSNs and may contribute to the enhanced susceptibility of D2 MSNs during HD progression