Double Dissociation of Attentional Resources: Prefrontal Versus Cingulate Cortices

Ng, Chi-Wing; Noblejas, Maria Imelda; Rodefer, Joshua S.; Smith, Christina B.; Poremba, Amy

doi:10.1523/jneurosci.2745-07.2007

Cited by 86 publications

(91 citation statements)

References 65 publications

(97 reference statements)

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“…1 D and E), suggesting impairments in cingulate, prelimbic/ infralimbic, and orbitofrontal function (19,20). The differences between obese and control rats on this task cannot be explained by lower motivation in the obese rats because the majority of animals in this group reached criterion, with seemingly more, not less, effort.…”

Section: Figmentioning

confidence: 93%

“…To further investigate the potential impairment of prefrontal function in obesity, we examined performance on an attentional set-shifting task (ASST), a test of behavioral flexibility (SI Appendix, Table S2), components of which depend on the rat cingulate, prelimbic/infralimbic, and orbitofrontal cortex but not the HIP (19)(20)(21). Obese rats performed poorly on the ASST compared with normal weight controls (F 1,12 = 20.45, P < 0.001) ( Fig.…”

Section: Significancementioning

confidence: 99%

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Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Bocarsly

Fasolino

Kane

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

194

151

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Obesity is a major public health problem affecting overall physical and emotional well-being. Despite compelling data suggesting an association between obesity and cognitive dysfunction, this phenomenon has received relatively little attention. Neuroimaging studies in obese humans report reduced size of brain regions involved in cognition, but few studies have investigated the cellular processes underlying cognitive decline in obesity or the influence of obesity on cognition in the absence of obesity-related illnesses. Here, a rat model of diet-induced obesity was used to explore changes in brain regions important for cognition. Obese rats showed deficits on cognitive tasks requiring the prefrontal and perirhinal cortex. Cognitive deficits were accompanied by decreased dendritic spine density and synaptic marker expression in both brain regions. Microglial morphology was also changed in the prefrontal cortex. Detrimental changes in the prefrontal cortex and perirhinal cortex occurred before metabolic syndrome or diabetes, suggesting that these brain regions may be particularly vulnerable to early stage obesity.O besity is a growing public health concern, affecting more than one-third of the United States adult population (1). Obesity increases the incidence of diabetes, vascular disease, and mental illness, all of which reduce quality of life and place a heavy financial burden on patients and society. Less recognized consequences of obesity are its deleterious effects on cognitive function. Individual cognitive performance, both rudimentary and scholastic, declines with increases in body mass and energy consumption (2-5). These deficits can be observed throughout life, from childhood to late adulthood. Obesity is also associated with an increased incidence of mild cognitive impairment and dementia in the elderly (6).Some evidence suggests that obese individuals have decreased overall brain volume (7), with further studies indicating more specific reductions in the volume of brain regions important for cognition, including the hippocampus, prefrontal cortex (PFC), and anterior cingulate (5,8,9). Few studies, however, have investigated the cellular and biochemical mechanisms that might underlie obesityinduced changes in brain volume and cognitive function.Although clinical studies strongly suggest that obesity produces cognitive impairment and brain atrophy, it is difficult to determine whether these changes arise from obesity itself or from conditions often associated with obesity, like metabolic syndrome, diabetes, and vascular disease. Such conditions, even in the absence of obesity, have been linked to cognitive dysfunction and decreases in brain volume (10-13). Little research has been done exploring the effects of obesity on brain structure and cognition in obese, but otherwise healthy, individuals. To investigate whether obesity in the absence of obvious illness alters brain structure and function, we used a rat model of dietinduced obesity to assess the PFC, the perirhinal cortex (PRC), and the hippocampus...

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Section: Figmentioning

confidence: 93%

Section: Significancementioning

confidence: 99%

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Bocarsly

Fasolino

Kane

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

194

151

View full text Add to dashboard Cite

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“…Acquisition of the concurrent discrimination task Extensive evidence indicates that the mPFC is not needed for simple discrimination learning (Ragozzino et al 1999b;Birrell and Brown 2000;Ragozzino et al 2003;Ng et al 2007). These studies suggested that the PFC is not needed for remembering which cues were associated with reward, but is instead only needed when the task requires behavioral flexibility, such as switching strategies or attentional set shifting.…”

Section: Methodsmentioning

confidence: 99%

“…Recently, a growing body of research has shown that the PFC is involved in similar functions in rodents. For example, medial prefrontal (mPFC) lesions cause impairments in a rodent adaptation of the Wisconsin card sorting task and the pattern of impairments is similar to those seen in humans (Ragozzino et al 1999b;Birrell and Brown 2000;Ng et al 2007). Like humans, the rats are unimpaired in learning the initial rule (e.g., respond according to one stimulus feature, such as odor), but they are severely impaired in learning to switch to a different stimulus feature (e.g., texture).…”

mentioning

confidence: 88%

“…Other studies have also shown that reversal learning is not impaired by mPFC lesions (Aggleton et al 1995;Floresco et al 2008). A number of authors have also emphasized the mPFC role in attentional processes in rats (Birrell and Brown 2000;Ng et al 2007). These studies demonstrate that the mPFC is critical in tasks that require rats to shift attention among competing stimulus features that indicate distinct behavioral responses.…”

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confidence: 95%

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The medial prefrontal cortex is critical for memory retrieval and resolving interference

et al. 2013

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The prefrontal cortex (PFC) is known to be critically involved in strategy switching, attentional set shifting, and inhibition of prepotent responses. A central feature of this kind of behavioral flexibility is the ability to resolve conflicting response tendencies, suggesting a general role of the PFC in resolving interference. If so, the PFC should also be involved in memory retrieval, which involves competition between potential retrieval targets. Moreover, the PFC should be needed whenever interference is high, regardless of the strategic or attentional requirements of the task. To test this hypothesis, we temporarily inactivated the mPFC with muscimol and tested rats on several olfactory learning tasks. Rats given muscimol were able to learn a few discrimination problems when they were learned one at a time. However, they were severely impaired when they had to learn and remember many odors concurrently. Rats given muscimol also suffered greater interference when learning two lists of conflicting odor discrimination problems. Additionally, temporary mPFC inactivation during the acquisition of one set of odor memories actually improved the ability to learn a new set of conflicting odor memories. This paradoxical release from interference suggests that the mPFC plays an important role in acquiring and promoting the long term retrieval of memories. These results suggest that the mPFC plays a general role in resolving interference and that this is a key aspect of behavioral flexibility.

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The influence of early maternal care on perceptual attentional set shifting and stress reactivity in adult rats

Sakhai

Saxton

Francis

2015

Developmental Psychobiology

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Stress influences a wide variety of outcomes including cognitive processing. In the rat, early life maternal care can influence developing offspring to affect both stress reactivity and cognitive processes in adulthood. The current study assessed if variations in early life maternal care can influence cognitive performance on a task, the ability to switch cognitive sets, dependent on the medial prefrontal cortex. Early in life, offspring was reared under High or Low maternal Licking conditions. As adults, they were trained daily and then tested on an attentional set-shifting task (ASST), which targets cognitive flexibility in rodents. Stress-sensitive behavioral and neural markers were assayed before and after the ASST. High and Low Licking offspring performed equally well on the ASST despite initial, but not later, differences in stress axis functioning. These results suggest that early life maternal care does not impact the accuracy of attentional set-shifting in rats. These findings may be of particular importance for those interested in the relationship between early life experience and adult cognitive function.ß 2015 Wiley Periodicals, Inc. Dev Psychobiol

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Double Dissociation of Attentional Resources: Prefrontal Versus Cingulate Cortices

Cited by 86 publications

References 65 publications

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

Obesity diminishes synaptic markers, alters microglial morphology, and impairs cognitive function

The medial prefrontal cortex is critical for memory retrieval and resolving interference

The influence of early maternal care on perceptual attentional set shifting and stress reactivity in adult rats

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