Prominent beta frequency oscillations appear in the basal ganglia of Parkinsons disease patients. The dynamical mechanisms by which these beta oscillations arise are unknown. Using mathematical models, we show that robust beta frequency rhythms can emerge from inhibitory interactions between striatal medium spiny neurons. The interaction between the intrinsic membrane M-current and the synaptic GABAa current provides a cellular-level interaction that promotes the formation of the beta frequency rhythm. Our modeling studies propose that the pathologic beta oscillations in Parkinsons disease may arise as an indirect eect of striatal dopamine loss on the striatal cholinergic system. Experimental testing of our model by infusion of the cholinergic agonist carbachol into normal, mouse striatum induced pronounced, reversible beta oscillations in the local eld potential. These results suggest the prominent beta oscillations in Parkinsons disease may be the result of an exaggeration of normal striatal network dynamics.