Decline of striatal dopamine release in parkin-deficient mice shown by ex vivo autoradiography
Version of Record online: 29 AUG 2006
Copyright © 2006 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 84, Issue 6, pages 1350–1357, 1 November 2006
How to Cite
Sato, S., Chiba, T., Nishiyama, S., Kakiuchi, T., Tsukada, H., Hatano, T., Fukuda, T., Yasoshima, Y., Kai, N., Kobayashi, K., Mizuno, Y., Tanaka, K. and Hattori, N. (2006), Decline of striatal dopamine release in parkin-deficient mice shown by ex vivo autoradiography. J. Neurosci. Res., 84: 1350–1357. doi: 10.1002/jnr.21032
- Issue online: 6 OCT 2006
- Version of Record online: 29 AUG 2006
- Manuscript Accepted: 29 JUN 2006
- Manuscript Revised: 25 MAY 2006
- Manuscript Received: 5 FEB 2006
Parkin is the causal gene of autosomal recessive juvenile parkinsonism (AR-JP). Dopamine (DA) metabolism has been linked to Parkinson's disease (PD). To understand the pathogenesis of AR-JP, we generated parkin-deficient mice to assess the status of DA signaling pathway and examine DA release and DA receptor by ex vivo autoradiography. Ex vivo autoradiography using [11C]raclopride showed a clear decrease in endogenous DA release after methamphetamine challenge in parkin-deficient mice. Furthermore, parkin deficiency was associated with considerable upregulation of DA (D1 and D2) receptor binding in vivo in the striatum and increased DA levels in the midbrain. Our results suggest that dopaminergic neurons could behave abnormally before neuronal death. © 2006 Wiley-Liss, Inc.