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The Journal of Neuroscience, February 23, 2005, 25(8):2132-2137; doi:10.1523/JNEUROSCI.3718-04.2005

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3,4-Dihydroxyphenylalanine Reverses the Motor Deficits in Pitx3-Deficient Aphakia Mice: Behavioral Characterization of a Novel Genetic Model of Parkinson's Disease

Dong-Youn Hwang,¹ Sheila M. Fleming,³ Paul Ardayfio,¹ Taylor Moran-Gates,² Hansoo Kim,¹ Frank I. Tarazi,² Marie-Francoise Chesselet,³ and Kwang-Soo Kim¹

¹Molecular Neurobiology Laboratory and ²Psychiatric Neuroscience Laboratory, McLean Hospital and Harvard Medical School, Belmont, Massachusetts 02478, and ³Departments of Neurology and Neurobiology, The David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California 90095-1769

Parkinson's disease (PD) is a neurodegenerative disease characterized by a loss of dopaminergic neurons in the substantia nigra. There is a need for genetic animal models of PD for screening and in vivo testing of novel restorative therapeutic agents. Although current genetic models of PD produce behavioral impairment and nigrostriatal dysfunction, they do not reproduce the loss of midbrain dopaminergic neurons and 3,4-dihydroxyphenylalanine (L-DOPA) reversible behavioral deficits. Here, we demonstrate that Pitx3-deficient aphakia (ak) mice, which have been shown previously to exhibit a major loss of substantia nigra dopaminergic neurons, display motor deficits that are reversed by L-DOPA and evidence of "dopaminergic supersensitivity" in the striatum. Thus, ak mice represent a novel genetic model exhibiting useful characteristics to test the efficacy of symptomatic therapies for PD and to study the functional changes in the striatum after dopamine depletion and L-DOPA treatment.

Key words: Parkinson's disease; substantia nigra; aphakia mouse; Pitx3; dopaminergic neuron; animal model

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Received Sep 8, 2004; revised January 11, 2005; accepted January 11, 2005.

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