Since GABA-ergic inhibitory control is needed to avoid aberrant processing within the dorsal horn after nerve injury [112], these results suggest that the transgenic murine model of dystonia exhibited delayed recovery from the sensitization process because of the role of torsinA in the activity of GABA-ergic and glutamatergic interneurons, the development of abnormalities in the neuronal nuclear membrane [113] and synaptogenesis [44]. Here, TOR1A is linked to Dystonia.