Effects of acute exercise on emotional memory.

Research has demonstrated beneficial effects of acute exercise on memory for neutral materials, such as word lists of neutral valence/low arousal. However, the impacts of exercise on emotional memory is less understood. Across three laboratory experiments in college students, we tested if acute exercise could enhance both neutral and emotional memory performance, anticipating a greater effect for emotional memory. We examined effects of exercise at varying intensities (Experiment 1: high-intensity; Experiment 2: low- and high-intensity; Experiment 3: moderate-intensity), of diverse modalities (Experiment 1: treadmill jogging; Experiment 2: cycling; Experiment 3: open-skill (racquetball) and closed-skill (treadmill jogging) exercise), and on emotional memory performance assessed at increasing levels of hippocampal dependency (Experiment 1: Y/N recognition task; Experiment 2: paired-associative recognition task; Experiment 3: cued-recall task). We found that, in all experiments, acute exercise did not significantly influence emotional or neutral memory performance relative to sedentary control conditions. However, we observed several noteworthy outcomes indicating that acute exercise may be linked to improvements in memory confidence and accuracy for central aspects of emotional memory stimuli, and that select exercise modalities (e.g. treadmill exercise) may also be associated with increased frequency of memory intrusions.

Time-dependent changes in hippocampal and striatal glycogen long after maze training in male rats.

Long-lasting biological changes reflecting past experience have been studied in and typically attributed to neurons in the brain. Astrocytes, which are also present in large number in the brain, have recently been found to contribute critically to learning and memory processing. In the brain, glycogen is primarily found in astrocytes and is metabolized to lactate, which can be released from astrocytes. Here we report that astrocytes themselves have intrinsic neurochemical plasticity that alters the availability and provision of metabolic substrates long after an experience. Rats were trained to find food on one of two versions of a 4-arm maze: a hippocampus-sensitive place task and a striatum-sensitive response task. Remarkably, hippocampal glycogen content increased while striatal levels decreased during the 30 days after rats were trained to find food in the place version, but not the response version, of the maze tasks. A long-term consequence of the durable changes in glycogen stores was seen in task-by-site differences in extracellular lactate responses activated by testing on a working memory task administered 30 days after initial training, the time when differences in glycogen content were most robust. These results suggest that astrocytic plasticity initiated by a single experience may augment future availability of energy reserves, perhaps priming brain areas to process learning of subsequent experiences more effectively.

Aerobic Fitness Unrelated to Acquisition of Spatial Relational Memory in College-Aged Adults.

While compelling evidence indicates that poorer aerobic fitness relates to impairments in retrieving information from hippocampal-dependent memory, there is a paucity of research on how aerobic fitness relates to the acquisition of such relational information. Accordingly, the present investigation examined the association between aerobic fitness and the rate of encoding spatial relational memory-assessed using a maximal oxygen consumption test and a spatial configuration task-in a sample of 152 college-aged adults. The findings from this investigation revealed no association between aerobic fitness and the acquisition of spatial relational memory. These findings have implications for how aerobic fitness is characterized with regard to memory, such that aerobic fitness does not appear to relate to the rate of learning spatial-relational information; however, given previously reported evidence, aerobic fitness may be associated with a greater ability to recall relational information from memory.

Prenatal fruit juice exposure enhances memory consolidation in male post-weanling Sprague-Dawley rats.

OBJECTIVES: Nutritional intake during gestation is known to impact health outcomes for progeny. Correlational evidence in humans suggests that increased fruit consumption of pregnant mothers enhances infant cognitive development. Moreover, wild-type Drosophila supplemented with a combination of orange and tomato juice showed robust enhancements in performance on an associative olfactory memory task. The current study aimed to experimentally test the effects of prenatal fruit juice exposure in a non-human, mammalian model of learning and memory. METHODS: Across three separate birth cohorts, pregnant rats were given access to diluted tomato and orange juice (N = 2 per cohort), with control rats (N = 2 per cohort) receiving only water, in addition to standard rodent chow, throughout the duration of gestation, ending at parturition. Following weaning, male offspring were tested for learning and memory in a spatial version of the circular water maze and an auditory-cued fear-conditioning task. RESULTS: All pregnant rats increased fluid and food intake over the gestational period. Fruit juice-fed pregnant rats had increased fluid intake compared to control pregnant rats. When testing progeny, there were no effects of prenatal fruit juice on spatial learning, while it appeared to impair learning in fear conditioning relative to controls. However, we measured significant enhancements in both spatial memory and conditioned fear memory in the prenatal fruit-juice group compared to controls. Measures of vigilance, in response to the conditioned cue, were increased in prenatal fruit rats compared to controls, suggesting less generalized, and more adaptive, anxiety behaviours. DISCUSSION: Our results corroborate the human and Drosophila findings of prenatal fruit effects on behaviour, specifically that prenatal fruit juice exposure may be beneficial for early-life memory consolidation in rats.

Differential effects of L- and D-lactate on memory encoding and consolidation: Potential role of HCAR1 signaling.

The process of memory consolidation is energy-demanding and brain energy deficits result in memory impairments. Indeed, L-lactate, a preferred neuronal energy substrate, enhances the formation of memory, while blockade of the neuronal uptake of L-lactate by either pharmacological means or using its enantiomer D-lactate, impairs memory. Beyond metabolism, both enantiomers of lactate also have signaling properties through the hydroxycarboxylic acid receptor 1 (HCAR1). Thus far, paradigms testing for an effect of lactate on memory modulation have ignored HCAR1 signaling while also mainly performing manipulations before learning and using intracranial administration techniques. Using an inhibitory avoidance (IA) memory protocol, the present study examined the effects of systemic administration of both L- and D-lactate as well as the specific HCAR1 agonist 3,5-dihydroxybenzoic acid (3,5-DHBA) across pre- and post-training periods. We found that post-training subcutaneous injections of either 3,5-DHBA or D-lactate significantly enhanced memory compared to saline controls, whereas L-lactate had no effect, suggesting that HCAR1 signaling in the absence of lactate metabolism supports memory consolidation processes. When administered 15 minutes prior to training, D-lactate and 3,5-DHBA impaired memory compared to saline controls. In contrast, L-lactate treated rats showed memory enhancements as compared to D-lactate-treated rats. Taken together, these results suggest different roles for lactate at different memory stages. It is likely that a metabolic role is at play during learning while HCAR1 signaling may play a greater role during consolidation.

The use of magnetic resonance spectroscopy for assessing the effect of diet on cognition.

Magnetic resonance spectroscopy (MRS) is an important tool for studying the effects of nutrition on brain health. MRS can be used to measure the concentrations of metabolites which are related to cognitive performance and sensitive to diet. These measurements can provide information about metabolic efficiency, plasma membrane stability, antioxidant status, and neurotransmitter availability. MRS can therefore be used to elucidate the biochemical mechanisms by which diet influences cognition, and to characterize the effects of nutritional interventions targeted to improve cognition.

Training-induced elevations in extracellular lactate in hippocampus and striatum: Dissociations by cognitive strategy and type of reward.

Recent evidence suggests that astrocytes convert glucose to lactate, which is released from the astrocytes and supports learning and memory. This report takes a multiple memory perspective to test the role of astrocytes in cognition using real-time lactate measurements during learning and memory. Extracellular lactate levels in the hippocampus or striatum were determined with lactate biosensors while rats were learning place (hippocampus-sensitive) or response (striatum-sensitive) versions of T-mazes. In the first experiment, rats were trained on the place and response tasks to locate a food reward. Extracellular lactate levels in the hippocampus increased beyond those of feeding controls during place training but not during response training. However, striatal lactate levels did not increase beyond those of controls when rats were trained on either the place or the response version of the maze. Because food ingestion itself increased blood glucose and brain lactate levels, the contribution of feeding may have confounded the brain lactate measures. Therefore, we conducted a second similar experiment using water as the reward. A very different pattern of lactate responses to training emerged when water was used as the task reward. First, provision of water itself did not result in large increases in either brain or blood lactate levels. Moreover, extracellular lactate levels increased in the striatum during response but not place learning, whereas extracellular lactate levels in the hippocampus did not differ across tasks. The findings from the two experiments suggest that the relative engagement of the hippocampus and striatum dissociates not only by task but also by reward type. The divergent lactate responses of the hippocampus and striatum in place and response tasks under different reward conditions may reflect ethological constraints tied to foraging for food and water.

Multivariate Associations of Fluid Intelligence and NAA.

Understanding the neural and metabolic correlates of fluid intelligence not only aids scientists in characterizing cognitive processes involved in intelligence, but it also offers insight into intervention methods to improve fluid intelligence. Here we use magnetic resonance spectroscopic imaging (MRSI) to measure N-acetyl aspartate (NAA), a biochemical marker of neural energy production and efficiency. We use principal components analysis (PCA) to examine how the distribution of NAA in the frontal and parietal lobes relates to fluid intelligence. We find that a left lateralized frontal-parietal component predicts fluid intelligence, and it does so independently of brain size, another significant predictor of fluid intelligence. These results suggest that the left motor regions play a key role in the visualization and planning necessary for spatial cognition and reasoning, and we discuss these findings in the context of the Parieto-Frontal Integration Theory of intelligence.

Use it and boost it with physical and mental activity.

One of the now classic tenets of neuroscience is that the brain retains a substantial amount of structural and functional plasticity throughout adulthood and old age. Enriching experiences that stimulate physical and mental activity produce robust changes in subsequent behaviors, including learning and memory, that tap a wide range of neural systems. In this article, we review evidence for cognitive priming with physical and mental exercise through a memory systems lens and present brain-derived neurotrophic factor (BDNF) signaling as one candidate neural mechanism for experience-dependent modulation of learning and memory. We highlight our recent findings showing that priming with voluntary exercise or with spontaneous alternation, a working memory task, enhances new learning of hippocampus-sensitive place, or striatum-sensitive response tasks. Blocking BDNF signaling with infusions of a BDNF receptor inhibitor into hippocampus or striatum just before training on place or response tasks, respectively, abrogated the benefits of priming regardless of the type of priming experience. These results suggest that enhanced BDNF signaling during learning may itself produce the cognitive benefits afforded by prior physical or mental activity.

Modulation of multiple memory systems: from neurotransmitters to metabolic substrates.

This article reviews evidence showing that neurochemical modulators can regulate the relative participation of the hippocampus and striatum in learning and memory tasks. For example, relative release of acetylcholine increases in the hippocampus and striatum reflects the relative engagement of these brain systems during learning of place and response tasks. Acetylcholine release is regulated in part by available brain glucose levels, which themselves are dynamically modified during learning. Recent findings suggest that glucose acts through astrocytes to deliver lactate to neurons. Brain glycogen is contained in astrocytes and provides a capacity to deliver energy substrates to neurons when needed, a need that can be generated by training on tasks that target hippocampal and striatal processing mechanisms. These results integrate an increase in blood glucose after epinephrine release from the adrenal medulla with provision of brain energy substrates, including lactate released from astrocytes. Together, the availability of peripheral and central energy substrates regulate the processing of learning and memory within and across multiple neural systems. Dysfunctions of the physiological steps that modulate memory--from hormones to neurotransmitters to metabolic substrates--may contribute importantly to some of the cognitive impairments seen during normal aging and during neurodegenerative diseases.