Keilhoff et al. (2004b) hypothesize that in their animal model of schizophrenia, ketamine may evoke its stimulating effect on hippocampal neurogenesis by blocking the NMDA receptor directly via reduction of c-Fos and c-Jun expression, leading to a depression of the AP1 transcription factor complex, and/or via a reduced NO production or an enhanced serotonergic activity. Here, JUN is linked to schizophrenia.