title: Systemic blockade of dopamine D2-like receptors increases high-voltage spindles in the globus pallidus and motor cortex of freely moving rats.
abstract: High-voltage spindles (HVSs) have been reported to appear spontaneously and widely in the cortical-basal ganglia networks of rats. Our previous study showed that dopamine depletion can significantly increase the power and coherence of HVSs in the globus pallidus (GP) and motor cortex of freely moving rats. However, it is unclear whether dopamine regulates HVS activity by acting on dopamine D₁-like receptors or D₂-like receptors. We employed local-field potential and electrocorticogram methods to simultaneously record the oscillatory activities in the GP and primary motor cortex (M1) in freely moving rats following systemic administration of dopamine receptor antagonists or saline. The results showed that the dopamine D₂-like receptor antagonists, raclopride and haloperidol, significantly increased the number and duration of HVSs, and the relative power associated with HVS activity in the GP and M1 cortex. Coherence values for HVS activity between the GP and M1 cortex area were also significantly increased by dopamine D₂-like receptor antagonists. On the contrary, the selective dopamine D₁-like receptor antagonist, SCH23390, had no significant effect on the number, duration, or relative power of HVSs, or HVS-related coherence between M1 and GP. In conclusion, dopamine D₂-like receptors, but not D₁-like receptors, were involved in HVS regulation. This supports the important role of dopamine D₂-like receptors in the regulation of HVSs. An siRNA knock-down experiment on the striatum confirmed our conclusion.
authors.affiliation: Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, People's Republic of China.
authors.forename: Chen
authors.initials: C
authors.lastname: Yang
authors.forename: Shun-Nan
authors.initials: SN
authors.lastname: Ge
authors.forename: Jia-Rui
authors.initials: JR
authors.lastname: Zhang
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Zhi-Qiang
authors.initials: ZQ
authors.lastname: Yan
authors.forename: Li-Jun
authors.initials: LJ
authors.lastname: Heng
authors.forename: Tian-Zhi
authors.initials: TZ
authors.lastname: Zhao
authors.forename: Wei-Xin
authors.initials: WX
authors.lastname: Li
authors.forename: Dong
authors.initials: D
authors.lastname: Jia
authors.forename: Jun-Ling
authors.initials: JL
authors.lastname: Zhu
authors.forename: Guo-Dong
authors.initials: GD
authors.lastname: Gao
mesh_terms: D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D058256:Brain Waves / Q000187:drug effects*; D065127:Dopamine D2 Receptor Antagonists; D055785:Gene Knockdown Techniques; D005917:Globus Pallidus / Q000187:drug effects / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D008124:Locomotion / Q000187:drug effects / Q000502:physiology; D008297:Male; D009044:Motor Cortex / Q000187:drug effects / Q000502:physiology*; D020891:Raclopride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D017448:Receptors, Dopamine D2 / Q000235:genetics / Q000378:metabolism
chemical_list: D001552:Benzazepines; D065127:Dopamine D2 Receptor Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; C534628:SCH 23390; D020891:Raclopride; D006220:Haloperidol