Psychopharmacology (2008) 199:77–88 in patients with schizophrenia. The detection of frontal sources only in EEG and not in MEG recordings is in line with the assumption that these sources are either predomi- nantly radial in orientation or located deeply in the brain (Rinne et al. 2000; Waberski et al. 2001). Nevertheless, even though several studies support a frontal lobe involvement in MMN generation (for a review, see Näätänen et al. 2007), we cannot exclude that the frontal source is simply an artifact due to the inverse problem of source analyses. The lack of influence on peak amplitude and latency of N1 and the predominant reduction in MMN activity after duration deviants in the NMDA antagonist model of psychosis are in line with observations in schizophrenic patients. It is noteworthy that recent studies reported an association between MMN deficits and poor functioning in schizophrenia (Light and Braff 2005a, b). These reports are in line with the psychological findings in our study, which suggest that the NMDA antagonist state (S-ketamine) is an appropriate model for psychoses with prominent negative symptoms (Gouzoulis-Mayfrank et al. 2005). Furthermore, two studies that investigated first-episode patients failed to find alterations in MMN activity (Salisbury et al. 2002; Umbricht et al. 2006). These findings suggest that the MMN impairment may develop in the ongoing course of the schizophrenic disorder. Hence, in terms of our model, the S-ketamine state may resemble not only the negative syndrome but also the more advanced stages of schizophrenia. Unlike S-ketamine, the 5HT2A agonist DMT reduced the N1 peak amplitude. This finding is in line with the increase of the N1 amplitude after treatment with 5HT2A antagonists (Juckel et al. 2003). On the basis of the grand average data, DMT had no significant effect on MMN activity. However, regarding the sources of MMN, DMT diminished the MMN activity to frequency-deviant stimuli at the two right hemispheric sources (S1 and S3). Noteworthy, Umbricht et al. (2003a, b) also found a significant reduction in the N1 amplitude and a stronger effect on MMN to frequency compared to duration deviants after administration of the 5HT2A agonist hallucinogen psilocybin. However, we cannot exclude that the changes in MMN activity under DMT are confounded by the significant reduction in the N1 amplitude. Both drugs led to higher missing and error rates, particularly for “BX” errors, in the AX-CPT. Javitt et al. (2000) reported a similar AX-CPT response pattern in patients with schizophrenia (Javitt et al. 2000). This is in line with an impairment in the use of contextual informa- tion, as indicated by a selective deficit in the ability of schizophrenia patients to inhibit responses to targets following presentation of incorrect no-go cues (Cohen et al. 1999). Hence, in terms of the context-dependent visual information processing at an attention-dependent level, both 87 models of psychosis seem to match previous findings with schizophrenia patients. It must be acknowledged that our study has methodo- logical limitations mainly due to the absence of a blinded placebo condition and the small sample sizes for com- pleters, which limited the statistical power. These limita- tions and the rationale for our study design were discussed in detail in our previous publications (Gouzoulis-Mayfrank et al. 2005, 2006). Taken together, although methodological caveats have to be taken into account, the data from the present study suggest that the NDMA antagonist and the 5HT2A agonist models of psychosis share common features regarding both automatic and conscious attentional mech- anisms. However, in terms of the automatic acoustic MMN generation, the NMDA antagonist model of psychosis appears to be more close to the findings in schizophrenia, whereas in terms of the visual context-dependent AX-CPT, both drugs lead to a performance deficit pattern, which comes close to previous findings in schizophrenic patients. Acknowledgements This work was supported by a grant of the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG) to the last author (Project no. 6 of a DFG clinical researcher group KFO 112/1/-1, Go 717/5-1). Some of the results of this article form part of a doctoral thesis of the fourth author (C.S.) at the Medical Faculty of the RWTH Aachen. The authors thank P.D. Dr. Ilonka Kreitschmann-Andermahr, P.D. Dr. René Gobbelé, and Dipl.-Ing. Klaus Harke for their support to this work. Disclosure/conflict of interest All authors certify that there is no actual or potential financial interest in relation to the subject matter or materials discussed in this manuscript. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References Abi-Saab WM, D’Souza DC, Moghaddam B, Krystal JH (1998) The NMDA antagonist model for schizophrenia: promise and pitfalls. Pharmacopsychiatry 31(Suppl 2):104–109 Alho K, Tervaniemi M, Huotilainen M, Lavikainen J, Tiitinen H, Ilmoniemi RJ, Knuutila J, Naatanen R (1996) Processing of complex sounds in the human auditory cortex as revealed by magnetic brain response. Psychophysiol 33:369–375 Baldeweg T, Klugman A, Gruzelier JH, Hirsch SR (2002) Impairment in frontal but not temporal components of mismatch negativity in schizophrenia. Int J Psychophysiol 43:111–122 Catts SV, Shelley AM, Ward PB, Liebert B, McConaghy N, Andrews S et al (1995) Brain potential evidence for an auditory sensory memory deficit in schizophrenia. Am J Psychiatry 152:213–219 Cohen JD, Barch DM, Carter C, Servan-Schreiber D (1999) Context- processing deficits in schizophrenia: converging evidence from