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The Journal of Neuroscience, June 1, 2005, 25(22):5273-5279; doi:10.1523/JNEUROSCI.4893-04.2005

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Neurobiology of Disease
Neuropeptide Y Protects against Methamphetamine-Induced Neuronal Apoptosis in the Mouse Striatum

Nathalie Thiriet,^1 * Xiaolin Deng,^2 * Marcello Solinas,^1,3 Bruce Ladenheim,² Wendy Curtis,⁴ Steven R. Goldberg,³ Richard D. Palmiter,⁴ and Jean Lud Cadet²

¹Centre National de la Recherche Scientifique 6187, University of Poitiers, 86000 Poitiers, France, ²Molecular Neuropsychiatry Branch and ³Preclinical Pharmacology Section, Behavioral Neuroscience Branch, Department of Health and Human Services, National Institutes of Health-National Instituteon Drug Abuse, Intramural Research Program, Baltimore, Maryland 21224, and ⁴Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195

Methamphetamine (METH) is an illicit drug that causes neuronal apoptosis in the mouse striatum, in a manner similar to the neuronal loss observed in neurodegenerative diseases. In the present study, injections of METH to mice were found to cause the death of enkephalin-positive projection neurons but not the death of neuropeptide Y (NPY)/nitric oxide synthase-positive striatal interneurons. In addition, these METH injections were associated with increased expression of neuropeptide Y mRNA and changes in the expression of the NPY receptors Y₁ and Y₂. Administration of NPY in the cerebral ventricles blocked METH-induced apoptosis, an effect that was mediated mainly by stimulation of NPY Y₂ receptors and, to a lesser extent, of NPY Y₁ receptors. Finally, we also found that neuropeptide Y knock-out mice were more sensitive than wild-type mice to METH-induced neuronal apoptosis of both enkephalin- and nitric oxide synthase-containing neurons, suggesting that NPY plays a general neuroprotective role within the striatum. Together, our results demonstrate that neuropeptide Y belongs to the class of factors that maintain neuronal integrity during cellular stresses. Given the similarity between the cell death patterns induced by METH and by disorders such as Huntington's disease, our results suggest that NPY analogs might be useful therapeutic agents against some neurodegenerative processes.

Key words: amphetamines; cell death; NPY; neurodegenerative diseases; neuroprotection; Y₂ receptor

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Received Dec 18, 2003; revised April 6, 2005; accepted April 8, 2005.

This article has been cited by other articles:

				F. Agasse, L. Bernardino, H. Kristiansen, S. H. Christiansen, R. Ferreira, B. Silva, S. Grade, D. P.D. Woldbye, and J. O. Malva Neuropeptide Y Promotes Neurogenesis in Murine Subventricular Zone Stem Cells, June 1, 2008; 26(6): 1636 - 1645. [Abstract] [Full Text] [PDF]

				K. A. Horner, S. C. Westwood, G. R. Hanson, and K. A. Keefe Multiple High Doses of Methamphetamine Increase the Number of Preproneuropeptide Y mRNA-Expressing Neurons in the Striatum of Rat via a Dopamine D1 Receptor-Dependent Mechanism J. Pharmacol. Exp. Ther., October 1, 2006; 319(1): 414 - 421. [Abstract] [Full Text] [PDF]

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