RT Journal Article SR Electronic T1 3,4-Dihydroxyphenylalanine Reverses the Motor Deficits in Pitx3-Deficient Aphakia Mice: Behavioral Characterization of a Novel Genetic Model of Parkinson's Disease JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 2132 OP 2137 DO 10.1523/JNEUROSCI.3718-04.2005 VO 25 IS 8 A1 Dong-Youn Hwang A1 Sheila M. Fleming A1 Paul Ardayfio A1 Taylor Moran-Gates A1 Hansoo Kim A1 Frank I. Tarazi A1 Marie-Francoise Chesselet A1 Kwang-Soo Kim YR 2005 UL http://www.jneurosci.org/content/25/8/2132.abstract AB 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.