Visual paradigm community edition8/11/2023 For example, if felt digging medium was the positive stimuli in the previous stage and paper was the negative stimuli, now the reverse is true. At the reversal stage, the previously negative stimuli within one dimension (medium in this example) is now positive, which challenges the animal to ignore the positive stimuli from the previous stage. Two stages within the AST protocol measure aspects of cognitive flexibility: reversal and the extra-dimensional shift. This reinforced rule forms a cognitive set. This association is then reinforced in subsequent tasks where the type of digging medium and odor changes, but the paired association between medium and reward remains. For example, in the AST, animals will learn to pay attention and respond to the relevant cue ( i.e., digging medium) and ignore an irrelevant cue ( i.e., odor), by pairing a food reward with the medium. These deficits indicate a state of cognitive inflexibility or an impaired ability to shift attentional set.Īn attentional set is formed when a subject learns that a set of rules can be applied to complex stimuli in order to differentiate relevant from irrelevant cues. Analogous deficits have been shown in both non-human primates and rodents when lesions to the prefrontal cortex have been induced 1,6-8. More generally, these patients are described as having deficits in cognitive flexibility. While the ability to learn simple rules remains intact, deficits in learning to modify a response when the rules have changed are found in patients suffering from a variety of neuropsychiatric disorders ( i.e., schizophrenia, obsessive compulsive disorder, depression), neurodegenerative disorders ( i.e., Parkinson’s disease) and in patients with lesions to the pre-frontal cortex 5. AST is modeled after the intradimensional /extradimensional component of the Cambridge Neuropsychological Test Automated Battery (CANTAB) which is used to identify cognitive dysfunction in humans and non-human primates 3,4. The attentional set shifting task (AST) was developed as a measure of attention and cognitive flexibility in rats over a decade ago 1,2. The neural circuits underlying behavior during the AST are highly conserved across humans, nonhuman primates and rodents, providing excellent face, construct and predictive validity. Here we describe the adaptation of a behavioral assay, the attentional set shifting task (AST), to be performed in mice to assess prefrontal cortex mediated cognitive deficits. However, preclinical behavioral assays used to assess these deficits in mouse models which can be readily manipulated genetically and could provide the basis for studies of new treatment avenues have been underutilized. Functional neuroimaging studies and postmortem analysis of human brain tissue implicate the PFC as being a primary region of dysregulation in patients with these disorders. Deficits in cognitive function also represent the most difficult symptom domain to successfully treat, as serotonin reuptake inhibitors and tricyclic antidepressants have only modest effects. Cognitive impairment, particularly involving dysfunction of circuitry within the prefrontal cortex (PFC), represents a core feature of many neuropsychiatric and neurodevelopmental disorders, including depression, post-traumatic stress disorder, schizophrenia and autism spectrum disorder.
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