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The Attentional Set Shifting Task: A Measure of Cognitive Flexibility in Mice
Published on: February 4, 2015
Prenatal malnutrition leads to deficits in attentional set shifting and decreases metabolic activity in prefrontal
Jill A McGaughy1, Ana C Amaral, R Jarrett Rushmore
1Department of Psychology, University of New Hampshire, Durham, N.H., USA.
Insights
Prenatal protein malnutrition in rats impairs executive functions and reduces metabolic activity in key brain regions. This early-life nutritional deficiency leads to lasting cognitive rigidity, mirroring human developmental challenges.
Area of Science:
- Neuroscience
- Developmental Biology
- Nutritional Science
Background:
- Malnutrition affects over 25% of children globally, causing persistent cognitive and emotional deficits.
- Prenatal malnutrition's long-term impact on brain development and executive functions requires further investigation.
Purpose of the Study:
- To investigate the effects of prenatal protein malnutrition on executive functions in a rodent model.
- To assess metabolic activity in prefrontal cortex (PFC) subregions following prenatal protein deficiency.
Main Methods:
- Long-Evans rats were fed low (6% casein) or adequate (25% casein) protein diets pre-mating and during gestation.
- Offspring underwent behavioral testing for attentional set-shifting and reversal learning at postnatal day 90.
- Regional brain metabolic activity was measured using (14)C-2-deoxyglucose (2DG) in naive littermates.
Main Results:
- Prenatally malnourished rats exhibited cognitive rigidity, struggling with attentional set-shifting and reversal learning.
- Reduced metabolic activity was observed in prenatally malnourished rats within the prelimbic, infralimbic, anterior cingulate, and orbitofrontal cortices.
- Metabolic activity in the piriform cortex and superior colliculus remained comparable to controls.
Conclusions:
- Prenatal protein malnutrition induces significant cognitive deficits in attentional set-shifting and reversal learning in a rodent model.
- Early-life nutritional insult leads to altered metabolic function in PFC subregions critical for executive functions.
- Findings suggest a link between prenatal malnutrition and cognitive inflexibility, relevant to human developmental outcomes.
Abstract:
Globally, over 25% of all children under the age of 5 years experience malnutrition leading to cognitive and emotional impairments that can persist into adulthood and beyond. We use a rodent model to determine the impact of prenatal protein malnutrition on executive functions in an attentional set-shifting task and metabolic activity in prefrontal cortex (PFC) subregions critical to these behaviors. Long-Evans dams were provided with a low (6% casein) or adequate (25% casein) protein diet 5 weeks before mating and during pregnancy. At birth, the litters were culled to 8 pups and fostered to control dams on the 25% casein diet. At postnatal day 90, prenatally malnourished rats were less able to shift attentional set and reverse reward contingencies than controls, demonstrating cognitive rigidity. Naive same-sexed littermates were assessed for regional brain activity using the metabolic marker (14)C-2-deoxyglucose (2DG). The prenatally malnourished rats had lower metabolic activity than controls in prelimbic, infralimbic, anterior cingulate, and orbitofrontal cortices, but had comparable activity in the nearby piriform cortex and superior colliculus. This study demonstrates that prenatal protein malnutrition in a well-described animal model produces cognitive deficits in tests of attentional set shifting and reversal learning, similar to findings of cognitive inflexibility reported in humans exposed to early childhood malnutrition.
