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Dystrophin-deficient, dystrophic (dy2J/dy2J) and dystrophic-derived (dy/dy) mice have been used as animal models of Duchenne muscular dystrophy (DMD). The dy2J/dy2J and dy/dy mice have a severe muscular dystrophy and the dy/dy mice develop moderate muscle weakness. They die prematurely because of respiratory and heart complications. Both dy2J/dy2J and dy/dy mice have a reduction of body weight, muscle mass and muscle strength, increase of serum creatine kinase and histological alterations. In the present study, we have compared the dy2J/dy2J and dy/dy mice with the Fisher 344 (F344) rat. The F344 rat is a commonly used laboratory animal for genetic studies, toxicological studies, and drug tests. We investigated the expression levels of the glutamate receptor subunits NR1, NR2A and NR2B, and the subunits of the N-methyl-D-aspartate glutamate receptor (NMDAR), the gamma-aminobutyric acid type A receptor (GABAAR) and the substance P receptor (NK1), as well as the transient receptor potential vanilloid type 1 receptor (TRPV1) in three different tissues: brain, spinal cord and muscle. The expression levels were measured using real-time polymerase chain reaction (RT-PCR). The NMDAR expression levels were reduced in the brain and spinal cord of both dy2J/dy2J and dy/dy mice. In the dy2J/dy2J mouse the NR2A expression level was reduced in the brain, and the NR2B expression level was reduced in the brain and spinal cord. The NK1 receptor expression level was decreased in the spinal cord of the dy/dy mice. In the dy2J/dy2J and dy/dy mice, but not in the F344 rat, the TRPV1 receptor expression levels were increased in the spinal cord. The GABAAR expression levels were increased in the spinal cord

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