The striatum is critically important in motor, cognitive and emotional functions, as highlighted in neurological disorders such as Huntington’s disease (HD) where these functions are compromised. The R6/2 mouse model of HD shows progressive motor and cognitive impairments and alterations in striatal dopamine and glutamate release. To determine whether or not dopamine-dependent neuronal plasticity is also altered in the dorsolateral striatum of R6/2 mice, we compared long term potentiation (LTP) and long term depression (LTD) in striatal slices from R6/2 mice with that seen in slices from wild type (WT) mice. In adult WT mice (aged 8–19 weeks), frequency-dependent bidirectional plasticity was observed. High frequency stimulation (four 0.5 s trains at 100 Hz, inter-train interval 10 s) induced LTP (134±5% of baseline), while low frequency stimulation (4 Hz for 15 min) induced LTD (80±5% of baseline). LTP and LTD were significantly blocked by the N-methyl-d-aspartic acid (NMDA) receptor antagonist d(−)-2-amino-5-phosphonopentanoic acid (D-AP5) (to 93±6% and 103±8% of baseline respectively), indicating that they are both dependent on NMDA glutamate receptor activation. LTP was significantly blocked by the dopamine D₁ receptor antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH-23390) (98±8% of baseline), indicating that LTP is dependent on activation of dopamine D₁-type receptors, whereas LTD was not significantly different (90±7%). In adult R6/2 mice (aged 8–19 weeks), LTP was significantly reduced (to 110±4% of baseline), while LTD was not significantly different from that seen in WT mice (85±6%). These data show that R6/2 mice have impaired dopamine-dependent neuronal plasticity in the striatum. As dopamine-dependent plasticity is a proposed model of striatum-based motor and cognitive functions, this impairment could contribute to deficits seen in R6/2 mice.