The hippocampus plays a critical role in processing contextual information. Although age-related changes in the hippocampus are well documented in humans, nonhuman primates, and rodents, few studies have examined contextual learning deficits in old rats. The present study investigated age-related differences in contextual associative learning in young (6 mo) and old (24 mo) rats using olfactory stimuli. Stimuli consisted of common odors mixed in sand and placed in clear plastic cups. Testing was conducted in two boxes that represented two different contexts (Context 1 and Context 2). The contexts varied based on environmental features of the box such as color (black vs. white), visual cues on the walls of the box, and flooring texture. Each rat was simultaneously presented with two cups, one filled with Odor A and one filled with Odor B in each context. In Context 1, the rat received a food reward for digging in the cup containing Odor A, but did not receive a food reward for digging in the cup containing Odor B. In Context 2, the rat was rewarded for digging in the cup containing Odor B, but did receive a reward for digging in the cup containing Odor A. Therefore, the rat learned to associate Context 1 with Odor A and Context 2 with Odor B. The rat was tested for eight days using the same odor problem throughout all days of testing. The results showed no significant difference between young and old rats on the first two days of testing; however, young rats significantly outperformed old rats on Day 3. Young rats continued to maintain superior performance compared to old rats on Days 4-8. The results suggest that aging results in functional impairments in brain regions that support memory for associations between specific cues and their respective context.

Neutrophil spontaneous apoptosis, a process crucial for immune regulation, is mainly controlled by alterations in reactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity; while acute severe exercise (ASE) usually impedes immunity, chronic moderate exercise (CME) improves it. This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercise group (n = 8) underwent 2 months of CME followed by 2 months of detraining. Additional ASE paradigms were performed at the end of each month. Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying neutrophil spontaneous apoptosis (annexin-V binding on the outer surface) along with redox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathione level, retarded spontaneous apoptosis and delayed mitochondria deterioration; iii) most effects of CME were unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore, the ASE effects on neutrophil spontaneous apoptosis were mimicked by adding exogenous H2O2, but not by suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted in acceleration of human neutrophil apoptosis, CME delayed neutrophil apoptosis by maintaining a reduced state for long periods of time even after detraining.

ASE and CME differentially affected neutrophil functions, whereas AME was ineffective. Moreover, the fact that CME improves neutrophil functions may partially explain why physically active subjects have a low risk of infection.

Key points• Exercise benefits the brain in many ways, e.g. promoting neuron repair and inhibiting neuroinflammation. However, current clinical practices often advise patients suffering head injury to rest during the post-traumatic period.• This study used a mouse model to investigate whether and how exercise retarded the brain structural and functional losses induced by a head impact.• An early moderate-exercise protocol (starting 2 days postimpact and lasting for 7 or 14 days) reversed the impact-induced rapid loss of recognition memory and prevented most of the delayed neuronal loss and neuroinflammation.• However, the same exercise protocol started 9 days postimpact was unable to restore deficits in the recognition memory, even though it still retarded the late-phase neuroinflammation.• These beneficial effects of exercise were probably mediated by the timely recovery of neurotrophic factors (brain-derived neurotrophic factor and mitogen-activated protein kinase phosphatase-1) in the injured brain.Abstract Closed-head injury (CHI) usually involves both physical damage of neurons and neuroinflammation. Although exercise promotes neuronal repair and suppresses neuroinflammation, CHI patients currently often remain resting during the post-traumatic period. This study aimed to investigate whether and how postinjury exercise benefited the brain structure and function in mice after CHI. Closed-head injury immediately caused an elevated neurological severity score, with rapid loss of object recognition memory, followed by progressive location-dependent brain damage (neuronal loss and activation of microglia in the cortex and hippocampus). An early exercise protocol at moderate intensity (starting 2 days postimpact and lasting for 7 or 14 days) effectively restored the object recognition memory and prevented the progressive neuronal loss and activation of microglia. However, if the exercise started 9 days postimpact, it was unable to recover recognition memory deficits. In parallel, early exercise intervention drastically promoted neurite regeneration, while late exercise intervention was much less effective. We also tested the possible involvement of brain-derived neurotrophic factor (BDNF) and mitogen-activated protein kinase phosphatase-1 (MKP-1) in the exercise-induced beneficial effects. Exercise gradually restored the impact-abolished hippocampal expression of BDNF and MPK-1, while oral administration of triptolide (a synthesis inhibitor of MKP-1 and an antagonist of nuclear factor-κB) before each bout of exercise blocked the restorative effects of exercise on MKP-1 and recognition memory, as well as the exercise-induced retardation of neuronal loss. Although triptolide treatment alone inhibited activation of microglia and maintained neuronal numbers, it did not recover the injury-hampered recognition memory. Overall, moderate exercise

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Chronic treadmill running in normotensive rats augmented the GABAergic system in both paraventricular nucleus and posterior hypothalamic area, resulting in lower resting blood pressure, heart rate and sympathetic tone under conscious unrestraint conditions. This study provides insight into mechanisms important for explaining how chronic exercise resets the resting blood pressure.

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CJ. Chronic treadmill exercise in rats delicately alters the Purkinje cell structure to improve motor performance and toxin resistance in the cerebellum. J Appl Physiol 113: 889-895, 2012. First published July 26, 2012 doi:10.1152/japplphysiol.01363.2011.-Although exercise usually improves motor performance, the underlying cellular changes in the cerebellum remain to be elucidated. This study aimed to investigate whether and how chronic treadmill exercise in young rats induced Purkinje cell changes to improve motor performance and rendered the cerebellum less vulnerable to toxin insults. After 1-wk familiarization of treadmill running, 6-wk-old male Wistar rats were divided into exercise and sedentary groups. The exercise group was then subjected to 8 wk of exercise training at moderate intensity. The rotarod test was carried out to evaluate motor performance. Purkinje cells in cerebellar slices were visualized by lucifer yellow labeling in single neurons and by calbindin immunostaining in groups of neurons. Compared with sedentary control rats, exercised rats not only performed better in the rotarod task, but also showed finer Purkinje cell structure (higher dendritic volume and spine density with the same dendritic field). The exercise-improved cerebellar functions were further evaluated by monitoring the long-lasting effects of intraventricular application of OX7-saporin. In the sedentary group, OX7-saporin treatment retarded the rotarod performance and induced ϳ60% Purkinje cell loss in 3 wk. As a comparison, the exercise group showed much milder injuries in the cerebellum by the same toxin treatment. In conclusion, exercise training in young rats increased the dendritic density of Purkinje cells, which might play an important role in improving the motor performance. Furthermore, as Purkinje cells in the exercise group were relatively toxin resistant, the exercised rats showed good motor performance, even under toxin-treated conditions. morphology; OX7-saporin; two-photon microscopy; running; motor function THE RELATIONSHIP BETWEEN PHYSICAL activity and brain functions has been widely investigated. In particular, physical activity in older subjects benefits their mental health by protecting the brain against age-related deterioration (6). Many exercise studies primarily focus on brain structural and functional changes related to cognitive improvements (15), with relatively few studies focusing on the motor performance. Consequently, although connections between cognitive deficits and age-associated brain differences have been elucidated, relationships with motor performance are less well understood. Interestingly, aging impacts brain structures and associated behaviors differentially, with the cerebellum showing earlier senescence than the hippocampus (31). As physically active older adults require less error monitoring and show improvements in motor performance (26), it is desirable to explore the beneficial effects of exercise on the cerebellum. Purkinje cells in aged rats show pronounced dendrite degener...