Purinergic Signalling

, Volume 7, Issue 1, pp 65–72

Astroglial P2X7 receptor current density increased following long-term exposure to rotenone

Original Article

DOI: 10.1007/s11302-011-9218-y

Cite this article as:
Gao, XF., Wang, W., Yu, Q. et al. Purinergic Signalling (2011) 7: 65. doi:10.1007/s11302-011-9218-y


The role of the interaction between neurons and glial cells in the pathogenesis of neurodegenerative diseases is gaining more attention. Neuroinflammation participates in the progressive nature of diverse neurologic diseases including Parkinson's disease, Alzheimer's disease and multiple sclerosis. Activated microglia release neurotoxic molecules, which take part in the neuroinflammatory responses. Astrocytes are also key players in these responses. Reactive astrocytes secrete inflammatory factors, including tumor necrosis factor-α (TNF-α). This secretion can be regulated by extracellular ATP mediated through P2X7 receptors. However, whether the activity of astrocytic P2X7 receptors changes in Parkinson’s disease and whether these changes would influence the secretion of inflammatory factors in astrocytes are still unclear. In our study, through immunocytochemistry, whole-cell patch clamp and ELISA assay, we found that P2X7 receptors were expressed in midbrain astrocytes, and that, rotenone, a Parkinson’s disease model used at a low concentration (2–20 nM) for 48 h increased the P2X7 receptor current density and thereby inhibited the secretion of TNF-α. Our research suggests that rotenone can regulate cytokine secretion of astrocytes through elevated P2X7 channel current density and, in turn, take part in the neuroinflammatory process in the rotenone Parkinson’s disease model.


Astrocytes Rotenone Purinergic P2X7 receptor Tumor necrosis factor-α 

Supplementary material

11302_2011_9218_Fig5_ESM.gif (26 kb)
Supplementary Fig. 1

The contrast pictures of cultured astrocytes. a The arrow indicates the hypertrophic astrocyte with long process. b The arrow indicates the astrocyte with flat and polygonal structures. Bar = 50 μm (GIF 25 kb)

11302_2011_9218_MOESM1_ESM.tif (4.3 mb)
High resolution image file (TIFF 4451 kb)

Copyright information

© Springer Science+Business Media B.V. 2011

Authors and Affiliations

  1. 1.Institute of Neuroscience and Key Laboratory of Molecular Neurobiology of Ministry of Education, Neuroscience Research Center of Changzheng HospitalSecond Military Medical UniversityShanghaiChina
  2. 2.Autonomic Neuroscience CentreUniversity College Medical School, Royal Free CampusLondonUK

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