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Abstract
Disturbances in cognitive functioning are among the most debilitating problems experienced by patients with major depression. Investigations of these deficits in animals help to extend and refine our understanding of human emotional disorder, while at the same time providing valid tools to study higher executive functions in animals. We employ the “learned helplessness” genetic rat model of depression in studying working memory using an eight arm radial maze procedure with temporal delay. This so-called delayed spatial win-shift task consists of three phases, training, delay and test, requiring rats to hold information on-line across a retention interval and making choices based on this information in the test phase. According to a 2×2 factorial design, working memory performance of thirty-one congenitally helpless (cLH) and non-helpless (cNLH) rats was tested on eighteen trials, additionally imposing two different delay durations, 30 s and 15 min, respectively. While not observing a general cognitive deficit in cLH rats, the delay length greatly influenced maze performance. Notably, performance was most impaired in cLH rats tested with the shorter 30 s delay, suggesting a stress-related disruption of attentional processes in rats that are more sensitive to stress. Our study provides direct animal homologues of clinically important measures in human research, and contributes to the non-invasive assessment of cognitive deficits associated with depression.
Highlights
Major depression is characterized by persistent sadness or low mood and loss of interests or pleasure as core symptoms [1]
Subjects We used 31 males of congenitally helpless and non-helpless rats from different litters of the 72nd, 73rd and 74th generations of the colonies bred at the Central Institute of Mental Health in Mannheim
Habituation Congenitally helpless and non-helpless rats did not differ with respect to the number of arms visited (F1,15 = 1.55, p.0.10) and the number of faecal boli dropped (F1,15 = 0.40, p.0.10)
Summary
Major depression is characterized by persistent sadness or low mood and loss of interests or pleasure as core symptoms [1]. Diagnostic criteria include cognitive impairments, such as reduced ability to concentrate and indecisiveness, but cognitive dysfunction associated with major depression has not received much attention until the last decade. Accumulating evidence indicates cognitive disturbances in the following domains: Affective processing, memory, negative feedback, and executive control, e.g. working memory [2,3,4,5]. In two recent studies applying cognitive bias procedures, the depressive-like phenotype of cLH rats was found to manifest in a negative response bias [14,15], indicating impaired affective processing similar to depressed patients. We aimed to test the hypothesis whether the observed depression-like symptoms in these rats are accompanied by deficits in executive control, focussing on working memory and attention
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