This article is a US Government work and, as such, is in the public domain in the United States of America.
Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease†
Article first published online: 3 JAN 2007
Copyright © 2007 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 85, Issue 4, pages 798–804, March 2007
How to Cite
Bäckman, C. M., Shan, L., Zhang, Y., Hoffer, B. J. and Tomac, A. C. (2007), Alterations in prodynorphin, proenkephalin, and GAD67 mRNA levels in the aged human putamen: Correlation with Parkinson's disease. J. Neurosci. Res., 85: 798–804. doi: 10.1002/jnr.21164
- Issue published online: 14 FEB 2007
- Article first published online: 3 JAN 2007
- Manuscript Revised: 1 NOV 2006
- Manuscript Accepted: 1 NOV 2006
- Manuscript Received: 19 SEP 2006
- Intramural Research Program of the NIDA, NIH
A real-time quantitative PCR approach was used to quantify mRNA levels corresponding to the neuropeptides enkephalin, dynorphin, and the 67-kDa isoform of glutamic acid decarboxylase (GAD67) in the human putamen from young and aged individuals as well as from aged patients affected by Parkinson's disease (PD). cDNA-specific primers were designed to amplify GAD67, proenkephalin (pENK), prodynorphin (pDYN), and the housekeeping genes glyceraldehydes-3-phosphate dehydrogenase (GAPDH) and guanine nucleotide binding protein, β-peptide 2-like I (GNB2LI). GAPDH and GNB2LI mRNA levels were similarly expressed among the groups and were therefore used as endogenous reference genes. Normalized data showed that mRNA levels for both pENK and pDYN were reduced in the putamen of aged controls and aged individuals affected by PD, compared with young controls. In addition, we showed that GAD67 mRNA levels did not change during aging and PD. Further analyses showed no differences in mRNA levels, for pENK, pDYN, or GAD67 mRNA, between PD patients and aged matched controls. These findings contrast with animal models of parkinsonism, for which expression of pDYN, pENK, and GAD67 mRNA has been reported to change after striatal dopamine denervation. Compensatory mechanisms and regional differences within the human putamen as well as the severity index of the disease, clinical diagnosis, and response to phalmacological therapy are possible reasons for these results. The present study suggests that alteration of neuropeptide pathways in the human putamen may be involved in the functional deterioration of parts of the extrapyramidal system during aging. © 2007 Wiley-Liss, Inc.