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Systemic Blockade of Dopamine D2-Like Receptors Increases High-Voltage Spindles in the Globus Pallidus and Motor Cortex of Freely Moving Rats.

Authors :
Yang, Chen
Ge, Shun-Nan
Zhang, Jia-Rui
Chen, Lei
Yan, Zhi-Qiang
Heng, Li-Jun
Zhao, Tian-Zhi
Li, Wei-Xin
Jia, Dong
Zhu, Jun-Ling
Gao, Guo-Dong
Source :
PLoS ONE. Jun2013, Vol. 8 Issue 6, p1-10. 10p.
Publication Year :
2013

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. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
19326203
Volume :
8
Issue :
6
Database :
Academic Search Index
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
88908098
Full Text :
https://doi.org/10.1371/journal.pone.0064637