title: Dopamine depletion increases the power and coherence of high-voltage spindles in the globus pallidus and motor cortex of freely moving rats.
abstract: Studies on patients with Parkinson's disease and in animal models have observed enhanced synchronization of oscillations in several frequency bands within and between the cortical-basal ganglia (BG) structures. Recent research has also shown that synchronization of high-voltage spindles (HVSs) in the cortex, striatum and substantia nigra pars reticulate is increased by dopamine depletion. However, more evidence is needed to determine whether HVS activity in the whole cortex-BG network represents homologous alteration following dopamine depletion. As the globus pallidus (GP) is in a central position to propagate and synchronize oscillations in the cortical-BG circuits, we employed local-field potentials and electrocorticogram to simultaneously record oscillations in the GP and primary (M1) and secondary (M2) motor cortices on freely moving 6-hydroxydopamine (6-OHDA) lesioned and control rats. Results showed that HVS episodes recorded from GP, and M2 and M1 cortex areas were more numerous and longer in 6-OHDA lesioned rats compared to controls. Relative power associated with HVS activity in the GP, and M2 and M1 cortices of 6-OHDA lesioned rats was significantly greater than that for control rats. Coherence values for HVS activity between the GP, and M2 and M1 cortex areas were significantly increased by dopamine depletion. Time lag between the M1 cortex HVS and GP HVS was significantly shorter for dopamine depleted than normal rats. Findings indicate a crucial rule for dopamine in the regulation of HVS activity in the whole cortical-BG circuit, and suggest a close relationship between abnormally synchronized HVS oscillations in the cortex-BG network and Parkinson's disease.
authors.affiliation: Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, People's Republic of China.
authors.forename: Shunnan
authors.initials: S
authors.lastname: Ge
authors.forename: Chen
authors.initials: C
authors.lastname: Yang
authors.forename: Min
authors.initials: M
authors.lastname: Li
authors.forename: Jiang
authors.initials: J
authors.lastname: Li
authors.forename: Xiaozan
authors.initials: X
authors.lastname: Chang
authors.forename: Jian
authors.initials: J
authors.lastname: Fu
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Chongwang
authors.initials: C
authors.lastname: Chang
authors.forename: Xuelian
authors.initials: X
authors.lastname: Wang
authors.forename: Junling
authors.initials: J
authors.lastname: Zhu
authors.forename: Guodong
authors.initials: G
authors.lastname: Gao
mesh_terms: D000818:Animals; D003344:Cortical Synchronization / Q000502:physiology*; D004298:Dopamine / Q000172:deficiency* / Q000502:physiology; D005917:Globus Pallidus / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009044:Motor Cortex / Q000378:metabolism / Q000503:physiopathology*; D009068:Movement / Q000502:physiology; D009434:Neural Pathways / Q000502:physiology; D020734:Parkinsonian Disorders / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D004298:Dopamine