There is evidence which suggests that alterations in the glutamatergic systems may contribute to the pathophysiology of depression,38 with elevated levels of glutamate observed in the cerebral cortex of depressed patients.39 Glutamate signalling is involved in neurological mechanisms implicated in the etiology of bipolar disorder (BD) such as brain development and synaptic plasticity.40 In post-mortem brain tissue from BD patients, altered levels of glutamate/glutamine, N-methyl-D-aspartate receptors41 and SLC1A2 protein and mRNA42 have been found. This evidence concerns the gene SLC1A2 and Behcet disease.