Preclinical studies have shown that pharmacological blockade of CB1R rendered animals more emotionally reactive and anxious [49, 50], susceptible to chronic stress-induced anhedonia [50], and to even manifest a depressive phenotype [51] as well as being liable to impairments in HPA axis regulation [52] reminiscent of neuroendocrine dysfunction observed in depression. This evidence concerns the gene CNR1 and depressive symptom measurement.