Glucose administration regulates many neural and behavioral processes in rodents, including learning and memory. Given the important role of glucose in brain function and the safety of glucose as a treatment, we have investigated the effects of glucose administration in humans of different ages. In previous work, we examined the effects of early-morning glucose consumption on cognitive functions in elderly individuals. In this population, glucose enhanced performance on specific measures, particularly on those tasks where mild age-related deficits appear (e.g., verbal declarative memory). Interestingly, glucose failed to enhance cognitive functions in young adults. Our recent work has examined three issues related to glucose enhancement of cognition: First, is glucose effective only in reversing impairments or can it also facilitate performance in highly functioning individuals? Second, are glucose effects dependent either on time of day or on interactions with other meals? Third, are typical breakfast foods as effective as glucose in enhancing cognitive performance? Our findings suggest that glucose can improve memory in highly functioning populations as it does in populations with deficits. However, enhancement by glucose may require sufficient levels of task difficulty and of blood glucose. In addition, like glucose, early morning consumption of cereal can improve performance on some cognitive tests. These results have important implications for the nature of glucose facilitation of memory and for the role of dietary factors in performance of many daily activities.
"Glucose, in turn, is taken from blood into the brain via active uptake mechanisms, where glucose acts directly on several brain sites to enhance memory formation. Like epinephrine, peripherally administered glucose enhances memory in laboratory rodents on a wide variety of tasks (for reviews: White, 1991; Gold, 2001, 2008; Korol, 2002; Messier, 2004), like epinephrine with an inverted-U dose-response curve as in Figure 2 (right; e.g., Gold, 1986; Hall and Gold, 1986). The glucose doses that enhance memory result in blood glucose levels comparable to those seen after epinephrine doses that enhance memory. "
[Show abstract][Hide abstract] ABSTRACT: This article reviews some of the neuroendocrine bases by which emotional events regulate brain mechanisms of learning and memory. In laboratory rodents, there is extensive evidence that epinephrine influences memory processing through an inverted-U relationship, at which moderate levels enhance and high levels impair memory. These effects are, in large part, mediated by increases in blood glucose levels subsequent to epinephrine release, which then provide support for the brain processes engaged by learning and memory. These brain processes include augmentation of neurotransmitter release and of energy metabolism, the latter apparently including a key role for astrocytic glycogen. In addition to up- and down-regulation of learning and memory in general, physiological concomitants of emotion and arousal can also switch the neural system that controls learning at a particular time, at once improving some attributes of learning and impairing others in a manner that results in a change in the strategy used to solve a problem.
Frontiers in Integrative Neuroscience 12/2012; 6:116. DOI:10.3389/fnint.2012.00116
"As seen in humans, rats and mice exhibit age-related impairments in learning and memory on many tasks. Often, the impairments are characterized in terms of rapid forgetting, in which aged rodents perform similarly to young adult rodents on memory tests soon after training, but have poor memory at later times as compared to young rodents (Barnes, 1991; Foster, 1999; Gold, 2005, 2001; Korol, 2002; Winocur, 1988). There are many examples of accelerated forgetting in aged rodents, with specific time courses that differ by task. "
[Show abstract][Hide abstract] ABSTRACT: This experiment examined whether age-related changes in CREB and pCREB contribute to the rapid forgetting seen in aged animals. Young (3-month-old) and aged (24-month-old) Fischer-344 rats received inhibitory avoidance training with a low (0.2 mA, 0.4 s) or moderate (0.5 mA, 0.5 s) foot shock; memory was measured 7 days later. Other rats were euthanized 30 min after training, and CREB and pCREB expression levels were examined in the hippocampus, amygdala, and piriform cortex using immunohistochemistry. CREB levels decreased with age in the hippocampus and amygdala. After training with either shock level, young rats exhibited good memory and increases in pCREB levels in the hippocampus and amygdala. Aged rats exhibited good memory for the moderate but not the low shock but did not show increases in pCREB levels after either shock intensity. These results suggest that decreases in total CREB and in pCREB activation in the hippocampus and amygdala may contribute to rapid forgetting in aged rats. After moderate foot shock, the stable memory in old rats together with absence of CREB activation suggests either that CREB was phosphorylated in a spatiotemporal pattern other than analyzed here or that the stronger training conditions engaged alternate mechanisms that promote long-lasting memory.
Mechanisms of ageing and development 03/2012; 133(5):291-9. DOI:10.1016/j.mad.2012.03.004 · 3.40 Impact Factor
"The increase in release of epinephrine without subsequent increases in circulating glucose levels suggests a breakdown in a neuroendocrine pathway important for modulating memory in old rats, potentially at the step in which glucose release from the liver is coupled to the binding of epinephrine. The uncoupling between peripheral epinephrine and glucose release may reduce the amount of glucose available to the brains of old rats during memory tasks and lead to the memory impairments and other cognitive changes seen in aged rats, mice and humans (Buckner, 2004; Chawla and Barnes, 2007; Disterhoft and Oh, 2006; Gazzaley and D'Esposito, 2007; Gold, 2005; Korol, 2002; Mattson et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: Increases in blood glucose levels are an important component of the mechanisms by which epinephrine enhances memory formation. The present experiments addressed the hypothesis that a dysfunction in the blood glucose response to circulating epinephrine contributes to age-related memory impairments. Doses of epinephrine and glucagon that significantly increased blood glucose levels in young adult rats were far less effective at doing so in 2-year-old rats. In young rats, epinephrine and glucose were about equally effective in enhancing memory and in prolonging post-training release of acetylcholine in the hippocampus. However, glucose was more effective than epinephrine in enhancing both memory and acetylcholine release in aged rats. These results suggest that an uncoupling between circulating epinephrine and glucose levels in old rats may lead to an age-related reduction in the provision of glucose to the brain during training. This in turn may contribute to age-related changes in memory and neural plasticity.
Neurobiology of aging 02/2009; 31(12):2136-45. DOI:10.1016/j.neurobiolaging.2008.12.003 · 5.01 Impact Factor
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