Event:

It becomes increasingly evident that cognitive disturbances are at the core of schizophrenia psychopathology. Search for animal models that model such cognitive impairments resulted in the development of a number of experimental approaches but nevertheless there was no success yet with advancing new treatments for schizophrenia that would be able to effectively target cognitive impairments. Also, it became clear that a simple boost to cognitive performance may not be beneficial. So, the preclinical quest continues. In this presentation, it will be argued that when modeled in laboratory animals, disease-related mechanisms may not necessarily produce functional impairments. Further, preclinical models may be designed to reflect a certain neurobiological mechanism rather than a specific cognitive domain known to be affected in schizophrenia. One of the examples to be discussed is glutamatergic hyperactivity as the mechanism that can be used to model cognitive impairments in laboratory animals. Glutamatergic signaling is critical for maintaining the optimal signal-to-noise ratio in cognitive networks and this function may be readily modeled preclinically and is of relevance to neurobiological mechanisms of impaired cognition in schizophrenia.