In the recent decades, a paradigmatic change in
psychosis research and treatment shifted attention toward the early and particularly the
prodromal stages of illness. Despite substantial progress with regard to the neuronal underpinnings of
psychosis development, the crucial biological mechanisms leading to manifest illness are yet insufficiently understood. Until today, one significant approach to elucidate the neurobiology of
psychosis has been the modeling of psychotic symptoms by
psychedelic substances in healthy individuals. These models bear the opportunity to evoke particular neuronal aberrations and the respective psychotic symptoms in a controlled experimental setting. In the present paper, we hypothesize that experimental psychiatry bears unique opportunities in elucidating the biological mechanisms of the
prodromal stages of
psychosis.
Psychosis risk symptoms are attenuated, transient, and often only retrospectively reported. The respective neuronal aberrations are thought being dynamic. The correlation of unstable psychopathology with observed neurofunctional disturbances is thus yet largely unclear. In modeling
psychosis, the experimental setting allows not only for evoking particular symptoms, but for the concomitant assessment of psychopathology, neurophysiology, and neuropsychology. Herein, the glutamatergic model will be highlighted exemplarily, with special emphasis on its potential contribution to the elucidation of
psychosis development. This model of
psychosis appears as candidate for modeling the prodrome by inducing psychotic-like symptoms in healthy individuals. Furthermore, it alters pre-attentive processing like the Mismatch Negativity, an electrophysiological component which has recently been identified as a potential predictive marker of
psychosis development. In summary, experimental psychiatry bears the potential to further elucidate the biological mechanisms of the
psychosis prodrome. A better understanding of the respective pathophysiology might assist in the identification of predictive markers, and the development of preventive treatments.