Synchronous oscillatory dynamics is frequently observed in the human brain.
We analyze the fine temporal structure of phase-locking in a realistic network
model and match it with the experimental data from parkinsonian patients. We
show that the experimentally observed intermittent synchrony can be generated
just by moderately increased coupling strength in the basal ganglia circuits
due to the lack of dopamine. Comparison of the experimental and modeling data
suggest that brain activity in Parkinson's disease resides in the large
boundary region between synchronized and nonsynchronized dynamics. Being on the
edge of synchrony may allow for easy formation of transient neuronal
assemblies
