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Abstract
Βeta oscillatory activity (human: 13–35 Hz; primate: 8–24 Hz) is pervasive within the cortex and basal ganglia. Studies in Parkinson’s disease patients and animal models suggest that beta-power increases with dopamine depletion. However, the exact relationship between oscillatory power, frequency and dopamine tone remains unclear. We recorded neural activity in the cortex and basal ganglia of healthy non-human primates while acutely and chronically up- and down-modulating dopamine levels. We assessed changes in beta oscillations in patients with Parkinson’s following acute and chronic changes in dopamine tone. Here we show beta oscillation frequency is strongly coupled with dopamine tone in both monkeys and humans. Power, coherence between single-units and local field potentials (LFP), spike-LFP phase-locking, and phase-amplitude coupling are not systematically regulated by dopamine levels. These results demonstrate that beta frequency is a key property of pathological oscillations in cortical and basal ganglia networks.
Dopamine tone modulation generates changes in beta oscillation physiology. Here the authors show beta frequency, and not power, coherence, phase-locking, or PAC is monotonically linked to dopamine tone and is likely the key property of pathological oscillations in cortical and basal ganglia networks.
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1 The Hebrew University–Hadassah Medical School, Department of Medical Neurobiology, Institute of Medical Research Israel–Canada (IMRIC), Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); The Hebrew University of Jerusalem, The Edmond and Lily Safra Center for Brain Sciences, Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); Weizmann Institute of Science, Department of Neurobiology, Rehovot, Israel (GRID:grid.13992.30) (ISNI:0000 0004 0604 7563)
2 The Hebrew University–Hadassah Medical School, Department of Medical Neurobiology, Institute of Medical Research Israel–Canada (IMRIC), Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); The Hebrew University of Jerusalem, The Edmond and Lily Safra Center for Brain Sciences, Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538)
3 University of Bordeaux, UMR 5293, IMN, Bordeaux, France (GRID:grid.462010.1); CNRS, UMR 5293, IMN, Bordeaux, France (GRID:grid.462010.1)
4 The Hebrew University–Hadassah Medical School, Department of Medical Neurobiology, Institute of Medical Research Israel–Canada (IMRIC), Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538)
5 Weizmann Institute of Science, Department of Neurobiology, Rehovot, Israel (GRID:grid.13992.30) (ISNI:0000 0004 0604 7563)
6 Hadassah University Hospital, Department of Neurosurgery, Jerusalem, Israel (GRID:grid.17788.31) (ISNI:0000 0001 2221 2926)
7 The Hebrew University–Hadassah Medical School, Department of Medical Neurobiology, Institute of Medical Research Israel–Canada (IMRIC), Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); Hebrew University Medical School, Jerusalem Mental Health Center, Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); Brigham and Women’s Hospital, Harvard Medical School, Department of Psychiatry, Boston, USA (GRID:grid.62560.37) (ISNI:0000 0004 0378 8294)
8 The Hebrew University–Hadassah Medical School, Department of Medical Neurobiology, Institute of Medical Research Israel–Canada (IMRIC), Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); The Hebrew University of Jerusalem, The Edmond and Lily Safra Center for Brain Sciences, Jerusalem, Israel (GRID:grid.9619.7) (ISNI:0000 0004 1937 0538); Hadassah University Hospital, Department of Neurosurgery, Jerusalem, Israel (GRID:grid.17788.31) (ISNI:0000 0001 2221 2926)