Fluctuations of extracellular glucose and lactate in the mouse primary visual cortex during visual stimulation

Béland-Millar, Alexandria; Messier, Claude

doi:10.1016/j.bbr.2018.02.018

Cited by 7 publications

(16 citation statements)

References 92 publications

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“…Interestingly, the changes observed by Boretius et al 83 were lowest in the cortex, which has been the main area of measurement in rodent fMRS studies. Another recent study in awake mice undergoing sustained visual stimulation 84 demonstrated a rise in extracellular Lac levels coupled with significant Glc decreases in their visual cortex. The authors also found important fluctuations of these changes, depending on the attention load as well as the blood and brain level availability of Glc.…”

Section: Quantification Of Metabolite Changesmentioning

confidence: 93%

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Proton functional magnetic resonance spectroscopy in rodents

Just

2020

NMR in Biomedicine

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Proton functional magnetic resonance spectroscopy ( 1 H-fMRS) in the human brain is able to assess and quantify the metabolic response due to localized brain activity.Currently, 1 H-fMRS of the human brain is complementary to functional magnetic resonance imaging (fMRI) and a recommended technique at high field strengths (>7 T) for the investigation of neurometabolic couplings, thereby providing insight into the mechanisms underlying brain activity and brain connectivity. Understanding typical healthy brain metabolism during a task is expected to provide a baseline from which to detect and characterize neurochemical alterations associated with various neurological or psychiatric disorders and diseases. It is of paramount importance to resolve fundamental questions related to the regulation of neurometabolic processes. New techniques such as optogenetics may be coupled to fMRI and fMRS to bring more specificity to investigations of brain cell populations during cerebral activation thus enabling a higher link to molecular changes and therapeutic advances. These rather novel techniques are mainly available for rodent applications and trigger renewed interest in animal fMRS. However, rodent fMRS remains fairly confidential due to its inherent low signal-to-noise ratio and its dependence on anesthesia. For instance, the accurate determination of metabolic concentration changes during stimulation requires robust knowledge of the physiological environment of the measured region of interest linked to anesthesia in most cases. These factors may also have a strong influence on B0 homogeneity. Therefore, a degree of calibration of the stimulus strength and duration may be needed for increased knowledge of the underpinnings of cerebral activity. Here, we propose an early review of the current status of 1 H-fMRS in rodents and summarize current difficulties and future perspectives.

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Section: Quantification Of Metabolite Changesmentioning

confidence: 93%

“…Boretius et al 83 reported that MED abolished the ISO‐induced rise in Lac due to its strong antiadrenergic effects. In awake mice under visual stimulation, Lac increased by 15% to 20% as assessed by electrochemical methods 84 . Notably, MED sedation has been used to mimic awake state 89…”

Section: Quantification Of Metabolite Changesmentioning

confidence: 99%

Proton functional magnetic resonance spectroscopy in rodents

Just

2020

NMR in Biomedicine

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“…To illustrate, critics of the glucose model have asserted that the brain’s energy expenditure exhibits little change from rest, concluding that because visual processing is a metabolically expensive process, if glucose supply was a constraint on brain function then “seeing would feel effortful” ( Kurzban et al, 2013 , p. 647). Sidestepping the unspoken assumption that phenomenological sensation is indicative of cortical metabolic activity, visual processing was the basis for some of the earliest measurements of task-associated increases in local brain metabolism, and a substantial body of evidence has accumulated that, while seeing may not ‘feel’ effortful, high levels of optical stimulation do lead to localized reductions in brain glucose in the visual cortex (e.g., Wagner et al, 1981 ; Cooper, 2002 ; Béland-Millar and Messier, 2018 ). The idea that increases in cognitive functioning do not cause substantial localized increases in the brain’s requirements for glucose would invalidate fMRI measurements, major in vivo imaging techniques, and centuries of work on brain fuel supply.…”

Section: Does Brain Energy Expenditure Decline As a Function Of Cognimentioning

confidence: 99%

“…Moreover, manipulations that affect local glucose supply directly modulate cognitive performance, and delivery of additional glucose both prevents glucose depletion and enhances cognitive performance (e.g., McNay et al, 2000 ). Even relatively simple processes such as visual processing, to return to the example process chosen by Kurzban et al (2013) , have been repeatedly shown to cause localized depletion of glucose from brain structures that process visual input: presentation of a novel visual stimulus depletes specifically visual cortex glucose ( Béland-Millar and Messier, 2018 ) while increasing local metabolism in a fashion very similar to hippocampal processing of a memory task; subsequent presentation of that same object (presumably requiring less processing) causes no such depletion, consistent with a task-difficulty explanation for depletion of local glucose. These and many other studies show very clearly that the first claim of the glucose model is likely correct: brain glucose is locally drained by difficult cognitive tasks and this depletion limits task performance.…”

Section: General Defense Of Brain Glucose Supply As a Constraint On Cmentioning

confidence: 99%

Mental Work Requires Physical Energy: Self-Control Is Neither Exception nor Exceptional

2018

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The brain’s reliance on glucose as a primary fuel source is well established, but psychological models of cognitive processing that take energy supply into account remain uncommon. One exception is research on self-control depletion, where debate continues over a limited-resource model. This model argues that a transient reduction in self-control after the exertion of prior self-control is caused by the depletion of brain glucose, and that self-control processes are special, perhaps unique, in this regard. This model has been argued to be physiologically implausible in several recent reviews. This paper attempts to correct some inaccuracies that have occurred during debate over the physiological plausibility of this model. We contend that not only is such limitation of cognition by constraints on glucose supply plausible, it is well established in the neuroscience literature across several cognitive domains. Conversely, we argue that there is no evidence that self-control is special in regard to its metabolic cost. Mental processes require physical energy, and the body is limited in its ability to supply the brain with sufficient energy to fuel mental processes. This article reviews current findings in brain metabolism and seeks to resolve the current conflict in the field regarding the physiological plausibility of the self-control glucose-depletion hypothesis.

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“…Rather, the decreases likely reflect increased brain utilization of glucose in response to the demands of information processing, i.e. uptake of extracellular glucose into neurons and astrocytes [66][67][68][69][70].…”

Section: Insert Figure 10 About Herementioning

confidence: 99%

Extracellular levels of glucose in the hippocampus and striatum during maze training for food or water reward in male rats

Scavuzzo

Newman

Gold

et al. 2020

Preprint

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Peripheral and central administration of glucose potently enhance cognitive functions. The present experiments examined changes in brain extracellular glucose levels while rats were trained to solve hippocampus-sensitive place or striatum-sensitive response learning tasks for food or water reward. During the first minutes of either place or response training, extracellular glucose levels declined in both the hippocampus and striatum, an effect not seen in untrained, rewarded rats. Subsequently, glucose increased in both brain areas under all training conditions, approaching asymptotic levels ~15-25 min into training. Compared to untrained-food controls, training with food reward resulted in significant increases in the hippocampus but not striatum; striatal levels exhibited large increases to food intake in both trained and untrained groups. In the rats trained to find water, glucose levels increased significantly above the values seen in untrained rats in both hippocampus and striatum. The present findings suggest that decreases in glucose early in training might reflect an increase in brain glucose consumption, perhaps triggering increased brain uptake of glucose from blood, as evident in the increases in glucose late in training. Together with past findings measuring lactate levels under the same conditions, the initial decreases in glucose may also stimulate increased production of lactate from astrocytes to support neural metabolism directly and/or to act as a signal to increase blood flow and glucose uptake into the brain.

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Fluctuations of extracellular glucose and lactate in the mouse primary visual cortex during visual stimulation

Cited by 7 publications

References 92 publications

Proton functional magnetic resonance spectroscopy in rodents

Proton functional magnetic resonance spectroscopy in rodents

Mental Work Requires Physical Energy: Self-Control Is Neither Exception nor Exceptional

Extracellular levels of glucose in the hippocampus and striatum during maze training for food or water reward in male rats

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