DescriptionAnimal models of mental disorders promote the development and evaluation of pharmacological interventions which ultimately improve the lives of the people who suffer from those disorder. The quality of life of people with schizophrenia is immensely affected by their disorder. While currently available treatments do reduce positive and negative symptoms in schizophrenia, they insufficiently improve cognitive symptoms and therefore inadequately improve quality of life. One hope is that animal models of schizophrenia can advance our understanding of the disorder and as a result lead the way to the discovery of new treatments. In this thesis I developed a nonhuman primate model of schizophrenia. One theory regarding schizophrenia is that some features in the disorder are the result of N-Methyl d-Aspartate receptor (NMDAR) hypofunction. Ketamine is an NMDAR antagonist and therefore serves as an experimental tool to investigate the consequences of NMDAR hypofunction. Therefore, I set out to test whether the effect of a low dose of ketamine on behavioral and electrophysiological aspects of visual perception in nonhuman primates (m. mulatta) matches findings in people with schizophrenia. The visual system of nonhuman primates is very close to that of humans which makes them uniquely suited to test predictions of the NMDAR hypofunction hypothesis on visual perception. I showed that after an injection of ketamine, visual contextual integration is reduced, in line with findings in schizophrenia. Furthermore, I showed that ketamine reduces steady state visual evoked responses, similar to what has been found in people with schizophrenia. Additionally, I developed a method to quantify gain, a ubiquitous feature of cortical processing, and show that ketamine reduces gain and gain control – processes that are impaired in schizophrenia. Finally, I discovered that full-screen flicker increases gain in nonhuman primates and replicated those findings in humans with EEG recordings. Together, my findings confirm that NMDAR hypofunction is a likely cause for altered visual perception in schizophrenia and show that ketamine is a useful tool to study NMDAR hypofunction in nonhuman primates. Moreover, my work suggests that full-screen flicker could remedy visual perception in schizophrenia and potentially other disorders that suffer from reduced gain control.