Preclinical models of DYT1 dystonia consist of transgenic mice expressing the gene encoding the human mutant (hMT) or the human wild-type (hWT) torsin A [31], presenting slower learning and reduced motor skills at 9 months of age, increased levels of μ opioid receptors, and an accumulation of glutamatergic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in striatal spiny neurons. This evidence concerns the gene TOR1A and Dystonia.