A potential mechanism is that atomoxetine, whose potentiation of extracellular levels of NA decreases spontaneous activity of LC neurons via α2-adrenoceptor stimulation in the LC [117], promotes a further decrease in the expression of Arc in the LC Arc+/TH+/zif268- neuronal ensemble in HD rats, thereby exacerbating their compulsivity. Here, TH is linked to Huntington disease.