Making Memories Matter

Gold, Paul E.; Korol, Donna L.

doi:10.3389/fnint.2012.00116

Cited by 29 publications

(24 citation statements)

References 160 publications

(195 reference statements)

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“…Many treatments enhance memory when administered soon after an experience and do so in retrograde time-dependent manner (McGaugh and Petrinovich, 1965; McGaugh, 1966, 2000; McGaugh and Roozendaal, 2009; Gold, 2008; Gold and Korol, 2012). These findings complement the extensive evidence that amnestic treatments can also act in time-dependent retrograde fashion.…”

Section: Memory Consolidation and Memory Modulationmentioning

confidence: 99%

“…Gold, 2006; Calabrese, 2008; Mattson, 2008; Gold and Korol, 2012). One suggestion is that the memory is erased by overly active mechanisms of plasticity, making and breaking connections too rapidly to retain memory for a new experience.…”

Section: Epinephrine and Memorymentioning

confidence: 99%

“…Bélanger et al, 2011; Magistretti, 2006; Pellerin et al, 2007; Gibbs et al, 2008; Pirttimaki and Parri, 2013; Bezzi and Volterra, 2011; Gold and Korol, 2012; Gold et al, 2013). These findings support a sequence by which glucose is taken into astrocytes for production of glycogen stores, with glycogenolysis and production of lactate initiated during learning by activation of neurotransmitter membrane receptors on astrocytes.…”

Section: Glucose Actions In the Brain Contributing To Memory Enhancementmentioning

confidence: 99%

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Regulation of memory – From the adrenal medulla to liver to astrocytes to neurons

Gold¹

2014

Brain Research Bulletin

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Epinephrine, released into blood from the adrenal medulla in response to arousing experiences, is a potent enhancer of learning and memory processing. This review examines mechanisms by which epinephrine exerts its effects on these cognitive functions. Because epinephrine is largely blocked from moving from blood to brain, it is likely that the hormone's effects on memory are mediated by peripheral actions. A classic effect of epinephrine is to act at the liver to break down glycogen stores, resulting in increased blood glucose levels. The increase in blood glucose provides additional energy substrates to the brain to buttress the processes needed for an experience to be learned and remembered. In part, it appears that the increased glucose may act in the brain in a manner akin to that evident in the liver, engaging glycogenolysis in astrocytes to provide an energy substrate, in this case lactate, to augment neuronal functions. Together, the findings reveal a mechanism underlying modulation of memory that integrates the physiological functions of multiple organ systems to support brain processes.

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Section: Memory Consolidation and Memory Modulationmentioning

confidence: 99%

Section: Epinephrine and Memorymentioning

confidence: 99%

Section: Glucose Actions In the Brain Contributing To Memory Enhancementmentioning

confidence: 99%

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Regulation of memory – From the adrenal medulla to liver to astrocytes to neurons

Gold¹

2014

Brain Research Bulletin

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“…There is now substantial evidence, as reviewed recently (Gold and Korol, 2012; Gold, 2014), showing that increased blood glucose levels in response to increases in epinephrine levels reflects a key mechanism linking epinephrine to memory. In a set of fundamental and classic experiments in biology, Sutherland and Rall (1960) showed that epinephrine activates hepatic adrenergic receptors to initiate the breakdown of glycogen to glucose with subsequent release of glucose into blood; it is these experiments that provided the first evidence for second-messenger systems in response to activation of cell membrane receptors.…”

Section: Background: Epinephrine and Glucose Modulation Of Memory Promentioning

confidence: 98%

Forgetfulness during aging: An integrated biology

Gold

Korol

2014

Neurobiology of Learning and Memory

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Age-related impairments in memory are often attributed to failures, at either systems or molecular levels, of memory storage processes. A major characteristic of changes in memory with increasing age is the advent of forgetfulness in old vs. young animals. This review examines the contribution of a dysfunction of the mechanisms responsible for modulating the maintenance of memory in aged rats. A memory-modulating system that includes epinephrine, acting through release of glucose from liver glycogen stores, potently enhances memory in young rats. In old rats, epinephrine loses its ability to release glucose and loses its efficacy in enhancing memory. Brain measures of extracellular levels of glucose in the hippocampus during memory testing show decreases in glucose in both young and old rats, but the decreases are markedly greater in extent and duration in old rats. Importantly, the old rats do not have the ability to increase blood glucose levels in response to arousal-related epinephrine release, which is retained and even increased in aged rats. Glucose appears to be able to reverse fully the increased rate of forgetting seen in old rats. This set of findings suggests that physiological mechanisms outside of the brain, i.e. changes in neuroendocrine functions, may contribute substantially to the onset of rapid forgetting in aged animals.

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“…The brain consumes about 60% of the glucose used up by the body. After a career testing substances that can enhance learning in humans and animal models, neurobiologist Paul Gold and colleagues found that one of the most effective is precisely glucose (Gold and Korol 2012;McNay and Gold 2002). In an experiment conducted with college students, ingestion of glucose led to increases of over 30% in participants' capacity to memorize text passages, in comparison with performance after ingestion of a control substance, the sweetener saccharin (Korol and Gold 1998).…”

Section: Nutritionmentioning

confidence: 99%

Physiology and assessment as low-hanging fruit for education overhaul

et al. 2016

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Physiology and assessment constitute major bottlenecks of school learning among students with low socioeconomic status. The limited resources and household overcrowding typical of poverty produce deficits in nutrition, sleep, and exercise that strongly hinder physiology and hence learning. Likewise, overcrowded classrooms hamper the assessment of individual learning with enough temporal resolution to make individual interventions effective. Computational measurements of learning offer hope for low-cost, fast, scalable, and yet personalized academic evaluation. Improvement of school schedules by reducing lecture time in favor of naps, exercise, meals, and frequent automated assessments of individual performance is an easily achievable goal for education.

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Making Memories Matter

Cited by 29 publications

References 160 publications

Regulation of memory – From the adrenal medulla to liver to astrocytes to neurons

Regulation of memory – From the adrenal medulla to liver to astrocytes to neurons

Forgetfulness during aging: An integrated biology

Physiology and assessment as low-hanging fruit for education overhaul

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