Reciprocally connected glutamatergic subthalamic nucleus (STN) and GABAergic external globus pallidus (GP) neurons normally exhibit weakly correlated, irregular activity but following the depletion of dopamine in Parkinson’s disease they express more highly correlated, rhythmic bursting activity. Patch clamp recording was utilized to test the hypothesis that dopaminergic modulation reduces the capability of GABAergic inputs to pattern "pathological" activity in STN neurons. Electrically evoked GABA_A receptor-mediated IPSCs exhibited activity-dependent plasticity in STN neurons, i.e. IPSCs evoked at frequencies between 1-50 Hz exhibited depression that increased with the frequency of activity. Dopamine, the D₂-like dopamine receptor agonist quinpirole and external media containing a low [Ca²⁺] reduced both the magnitude of IPSCs evoked at 1-50 Hz and synaptic depression at 10-50 Hz. Dopamine/quinpirole also reduced the frequency but not the amplitude of miniature IPSCs recorded in the presence of tetrodotoxin. D₁-like and D₄ agonists were ineffective and D_2/3 but not D₄ receptor antagonists reversed the effects of dopamine or quinpirole. Together these data suggest that presynaptic D2/3 dopamine receptors modulate the short-term dynamics of GABAergic transmission in the STN by lowering the initial probability of transmitter release. Simulated GABA_A receptor-mediated synaptic conductances representative of control and modulated transmission were then generated in STN neurons using the dynamic clamp technique. Dopamine-modulated transmission was less effective at resetting autonomous activity or generating rebound burst firing than control transmission. The data therefore support the conclusion that dopamine acting at presynaptic D₂-like receptors reduces the propensity for GABAergic transmission to generate correlated, bursting activity in STN neurons.