Abstract
The development of sophisticated, translatable mouse-based assays modeling the behavioral manifestations of neuropsychiatric diseases, such as schizophrenia, has lagged the advances in molecular and genomic techniques. Our laboratory has made efforts to fill this gap by investing in the development of novel assays, including adapting a touchscreen-based method for measuring cognitive and executive functions for use in mice. As part of these efforts, a recent study by Brigman et al. (2009) investigated the effects of subchronic phencyclidine treatment on mouse touchscreen-based pairwise visual discrimination and reversal learning. Here, we summarize the results of that study, and place them in the larger context of ongoing efforts to develop valid mouse “models” of schizophrenia, with a focus on reversal learning and other measures of cognitive flexibility. Touchscreen-based systems could provide a tractable platform for fully utilizing the mouse to elucidate the pathophysiology of cognitive inflexibility in schizophrenia and other neuropsychiatric disorders.
Highlights
The last decade has seen the mouse become one of the model species of choice for researchers studying brain function and neuropsychiatric diseases
As part of a larger research program to elucidate the role of glutamate in cognitive and executive functions, we have studied the effects of null mutations in various components of the glutamate system on the touchscreen-based method (Brigman et al, 2008; Karlsson et al, 2008; Wiedholz et al, 2008; Karlsson et al, 2009)
Concluding remarks The Brigman et al data raise some interesting questions for further studies examining the effects of subchronic PCP on reversal in the touchscreen system
Summary
The last decade has seen the mouse become one of the model species of choice for researchers studying brain function and neuropsychiatric diseases. This trend has been catalyzed by two key scientific advances during this period: the emergence of techniques for precisely manipulating the mouse genome, such as gene-targeting (Capecchi, 2005), and the sequencing of the human genome (International Human Genome Sequencing Consortium, 2004). The development of sophisticated, translatable mouse-based assays for the behavioral manifestations of schizophrenia has lagged the advances in molecular and genomic techniques. Contrary to a commonly voiced opinion, we do not believe that this is because mice are “not smart enough” to perform complex behavioral, cognitive, assays, but rather that an adequate investment of time and effort has not been put into adapting and validating procedures for the mouse
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