Treatment of Fmr1 KO mice (an animal model of Fragile X syndrome), exhibiting an hyper-excitability and a GABAergic dysfunction in the basolateral nucleus of the amygdala, with gaboxadol (THIP), a selective agonist at δ subunits containing perisynaptic or extrasynaptic GABAA receptors, results in an increased GABAA-mediated tonic conductance and in beneficial effects on learning deficits and behavioral disturbances linked to this disorder. This evidence concerns the gene FMR1 and fragile X syndrome.