Exercise modifies α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor expression in striatopallidal neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse.
作者： N. Kintz , G.M. Petzinger , G. Akopian , S. Ptasnik , C. Williams
DOI: 10.1002/JNR.23260
关键词:
摘要: The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid-type glutamate receptor (AMPAR) plays a critical role in modulating experience-dependent neuroplasticity, and alterations AMPAR expression may underlie synaptic dysfunction disease pathophysiology. Using the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of dopamine (DA) depletion, our previous work showed exercise increases total GluA2 subunit contribution GluA2-containing channels MPTP mice. purpose this study was to determine whether exercise-dependent changes after are specific striatopallidal (D2R) or striatonigral (D1R) medium spiny neuron (MSN) striatal projection pathways. Drd2-eGFP-BAC transgenic mice were used delineate differences between D2R-MSNs D1R-MSNs. Striatal assessed by immunohistochemical (IHC) staining, Western immunoblotting (WB) preparations enriched for postsynaptic density (PSD), current–voltage relationship MSNs. We found DA depletion results emergence GluA2-lacking AMPARs selectively that reverses effect Exercise-induced observed associated with GluA1 protein, D2R-MSN cell surface expression, restoration corticostriatal plasticity. Mechanisms regulating provide innovative therapeutic targets increase efficacy treatments basal ganglia disorders, including Parkinson's disease. © 2013 Wiley Periodicals, Inc.
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