Neural synchrony in the basal ganglia, especially in the beta frequency band (13-30 Hz), is a hallmark of Parkinson's disease and considered as antikinetic. In contrast, the healthy basal ganglia show low levels of synchrony. It is currently unknown where synchrony and oscillations arise in the parkinsonian brain and how they are transmitted through the basal ganglia, as well as what makes them dependent on dopamine. The external part of the globus pallidus has recently been identified as a hub nucleus in the basal ganglia, possessing intrinsic inhibitory connections and possibly also gap junctions. In this study, we show that in a conductance-based network model of the basal ganglia, the combination of sparse, high-conductance inhibitory synapses and sparse, low-conductance gap junctions in the external part of the globus pallidus could effectively desynchronize the whole network. However, when gap junction coupling became strong enough, the effect was impeded and activity synchronized. In particular, sustained periods of beta coherence occurred between some neuron pairs. As gap junctions can change their conductance with the dopamine level, we suggest pallidal gap junction coupling as a mechanism contributing to the development of beta synchrony in the parkinsonian basal ganglia.