Attentional Set-Shifting Test (AST) - Reaching test stage successful criterion number

General Details:

Name:
Attentional Set-Shifting Test (AST) - Reaching test stage successful criterion number
Steward:
NINDS
Definition:
The number of correct responses needed to move to the next stage, as part of Attentional Set-Shifting Test (AST)
Registration Status:
Qualified

Permissible Values:

Data Type:
Number
Unit of Measure:
Ids:
Value Code Name Code Code System Code Description

Designations:

Designation:
Attentional Set-Shifting Test (AST) - Reaching test stage successful criterion number
Tags:
Designation:
Reaching test stage successful criterion number
Tags:
Preferred Question Text

Designations:

Definition:
The number of correct responses needed to move to the next stage, as part of Attentional Set-Shifting Test (AST)
Tags:
Short Description,Definition

Reference Documents:

ID:
Title:
Old dog, new tricks: the attentional set-shifting test as a novel cognitive behavioral task after controlled cortical impact injury.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=24397572
Provider Org:
Language Code:
en-us
Document:
Cognitive impairment associated with prefrontal cortical dysfunction is a major component of disability in traumatic brain injury (TBI) survivors. Specifically, deficits of cognitive flexibility and attentional set-shifting are present across all levels of injury severity. Though alterations in spatial learning have been extensively described in experimental models of TBI, studies investigating more complex cognitive deficits are relatively scarce. Hence, the aim of this preclinical study was to expand on this important issue by evaluating the effect of three injury levels on executive function and behavioral flexibility performance as assessed using an attentional set-shifting test (AST). Isoflurane-anesthetized male rats received a controlled cortical impact (CCI) injury (2.6, 2.8, and 3.0 mm cortical depth at 4 m/sec) or sham injury, whereas an additional group had no surgical manipulation (naïve). Four weeks postsurgery, rats were tested on the AST, which involved a series of discriminative tasks of increasing difficulty, such as simple and compound discriminations, stimulus reversals, and intra- and extradimensional (ED) shifts. TBI produced accompanying impact depth-dependent increases in cortical lesion volumes, with the 3.0-mm cortical depth group displaying significantly larger injury volumes than the 2.6-mm group (p=0.05). Further, injury severity-induced deficits in ED set-shifting and stimulus reversals, as well as increases in total response error rates and total set loss errors, were observed. These novel findings demonstrate executive function and behavioral flexibility deficits in our animal model of CCI injury and provide the impetus to integrate the AST in the standard neurotrauma behavioral battery to further evaluate cognitive dysfunction after TBI. Ongoing experiments in our laboratory are assessing AST performance after pharmacological and rehabilitative therapies post-TBI, as well as elucidating possible mechanisms underlying the observed neuropsychological deficits.
ID:
Title:
Behavioural assays to model cognitive and affective dimensions of depression and anxiety in rats.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=18673411
Provider Org:
Language Code:
en-us
Document:
Animal models have been used extensively to investigate neuropsychiatric disorders, such as depression, and their treatment. However, the aetiology and pathophysiology of many such disorders are largely unknown, which makes validation of animal models particularly challenging. Furthermore, many diagnostic symptoms are difficult to define, operationalize and quantify, especially in experimental animals such as rats. Thus, rather than attempting to model complex human syndromes such as depression in their entirety, it can be more productive to define and model components of the illness that may account for clusters of co-varying symptoms, and that may share common underlying neurobiological mechanisms. In preclinical investigations of the neural regulatory mechanisms linking stress to depression and anxiety disorders, as well as the mechanisms by which chronic treatment with antidepressant drugs may exert their beneficial effects in these conditions, we have employed a number of behavioural tests in rats to model specific cognitive and anxiety-like components of depression and anxiety disorders. In the present study, we review the procedures for conducting four such behavioural assays: the attentional set-shifting test, the elevated-plus maze, the social interaction test and the shock-probe defensive burying test. The purpose is to serve as a guide to the utility and limitations of these tools, and as an aid in optimising their use and productivity.
ID:
Title:
Beneficial effects of desipramine on cognitive function of chronically stressed rats are mediated by alpha1-adrenergic receptors in medial prefrontal cortex.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=20417676
Provider Org:
Language Code:
en-us
Document:
Chronic stress is a risk factor for many psychopathological conditions, including depression and anxiety disorders. Cognitive impairments associated with prefrontal cortical dysfunction are a major component of such illnesses. Using an attentional set-shifting test (AST), we have previously shown that elevating noradrenergic activity in rat medial prefrontal cortex (mPFC) can facilitate cognitive set-shifting, and that chronic unpredictable stress (CUS) caused set-shifting deficits. It is not known, however, if noradrenergic modulatory function is compromised by chronic stress, perhaps contributing to the stress-induced cognitive deficit. Thus, the first study investigated whether acutely elevating noradrenergic activity in mPFC still enhances cognitive function after chronic stress. As previously demonstrated, CUS impaired cognitive set-shifting on the AST. This deficit was abolished by acute systemic administration of the alpha(2)-adrenergic autoreceptor antagonist, atipamezole. Microdialysis revealed no differences in extracellular norepinephrine (NE) levels in mPFC of CUS-exposed and unstressed control rats at baseline or during behavioral testing, and comparable increases after atipamezole. In the second experiment, rats were treated chronically with the selective NE reuptake blocker, desipramine, during the CUS treatment through behavioral testing. Again, CUS impaired cognitive set-shifting in vehicle-treated rats, and chronic desipramine treatment prevented such deficits. Acute blockade of post-synaptic alpha(1)-adrenergic receptors in mPFC prior to testing blocked the beneficial effect of desipramine on cognitive set-shifting. These results suggest that desipramine restores cognitive set-shifting capability that has been compromised by chronic stress by activating alpha(1)-adrenergic receptors in the mPFC. Thus, noradrenergic modulatory capability in mPFC remains intact after CUS, and this represents one possible substrate by which antidepressants may exert their beneficial effects in the treatment of depression.
ID:
Title:
Old dog, new tricks: the attentional set-shifting test as a novel cognitive behavioral task after controlled cortical impact injury.
URI:
https://www.ncbi.nlm.nih.gov/pubmed/?term=24397572
Provider Org:
Language Code:
en-us
Document:

Properties:

Key:
Keywords
Value:
AST;Preclinical;Executive_function
Key:
Guidelines/Instructions
Value:
The number of correct responses needed to move to the next stage. Typically 6 consecutive correct responses are needed to move to next stage
Key:
Notes
Value:
Specific for rat and mice only

Identifiers:

Source:
NLM
Id:
Q1GgdiMj4
Version:
1.0
Source:
BRICS Variable Name
Id:
ASTTestStageReachSuccNum
Version: