Physiology & Behavior最新文献

Alzheimer's Disease (AD) is a debilitating neurocognitive disorder with an unclear underlying mechanism. Recent studies have implicated gut microbiota dysbiosis with the onset and progression of AD. The connection between gut microbiota and AD can significantly affect the prevention and treatment of AD patients. This systematic review summarizes primary outcomes of human and mouse AD models concerning gut microbiota alterations. A systematic literature search in February through March 2023 was conducted on PubMed, Embase, and Web of Science. We identified 711 as potential manuscripts of which 672 were excluded because of irrelevance to the identified search criteria. Primary outcomes include microbiota compositions of control and AD models in humans and mice. In total, 39 studies were included (19 mouse and 20 human studies), published between 2017 and 2023. We included studies involving well-established mice models of AD (5xFAD, 3xTg-AD, APP/PS1, Tg2576, and APPPS2) which harbor mutations and genes that drive the formation of Aß plaques. All human studies were included on those with AD or mild cognitive impairment. Among alterations in gut microbiota, most studies found a decreased abundance of the phyla Firmicutes and Bifidobacteria, a genus of the phylum Actinomycetota. An increased abundance of the phyla Bacteroidetes and Proteobacteria were identified in animal and human studies. Studies indicated that gut microbiota alter the pathogenesis of AD through its impact on neuroinflammation and permeability of the gastrointestinal tract. The ensuing increase in blood-brain barrier permeability may accelerate Aβ penetrance and formation of neuritic plaques that align with the amyloid hypothesis of AD pathogenesis. Further studies should assess the relationship between gut microbiota and AD progression and therapy preserving beneficial gut microbiota.

Objective: Evidence suggests that acute exercise is an effective way for improving inhibition control, however, the effect of different types of Acute Aerobic Exercise and Inhibitory Control (IC) remains unclear.

Method: Using a crossover design, 25 participants (M = 20.20year, SD=0.91) completed 20 min of interventions at 1) moderate intensity exercise, 2) moderate intensity exercise with high cognitive demand (high cognitive-demand exercise), 3) moderate intensity exercise with high physical demand (high physical-demand exercise), and 4) rest condition (low physical and cognitive demand) in a counterbalanced way. Flanker task was completed before and after each intervention to evaluate their inhibitory control ability.

Results: The four interventions significantly reduce reaction times for both congruent and incongruent trials with Flanker task (all P < 0.05). Compared to acute moderate intensity exercise, high physical-demand exercise induced a greater reduction in reaction times for both trial types, whereas high cognitive-demand exercise led to faster reaction times in incongruent trials.

Conclusion: Although each intervention effectively enhanced inhibitory control, the exercise demanding high cognitive and physical effort contributed to a more pronounced improvement in inhibitory control performance. This indicates that both increased physical and cognitive engagement can significantly improve the level of inhibitory control in young adults.

Exposure to artificial light at night (ALAN) disrupts natural darkness and desynchronizes daily rhythms in physiological processes and behavior. Previously, in rats, we have shown that dim ALAN disturbed the central circadian control and the temporal organization of behavior, and hormonal and metabolic pathways. The measurements of undisturbed daily behavioral (locomotor activity, feeding and drinking) patterns revealed reduced amplitudes and a transitory activity peak in the middle of the light (i.e. resting) period. Recent studies indicated that time-restricted feeding during the active period (TRFd) can strengthen daily rhythms and improve metabolic health. Therefore, the aim of our study was to prevent the dim ALAN-induced attenuation of daily behavioral rhythms by applying TRFd. Male Wistar rats were kept in a 12/12 light/dark cycle in metabolic cages for one week with free access to food and water. After acclimation, rats were divided into two groups: 1) ad libitum food or 2) time-restricted food during the dark period. After one week, both groups were exposed to dim ALAN for two weeks. Despite the enhanced amplitude of the daily feeding rhythm in TRFd animals, ALAN still suppressed the rhythm of locomotor activity, induced the extra peak during the resting period and reduced the bimodal pattern during the night. Furthermore, TRFd did not prevent the drop in anticipatory thirst caused by ALAN at the end of the active period. In conclusion, TRFd was not able to fully prevent the weakning of daily behavioral rhythms by dim ALAN.

Introduction: Despite emerging evidence on oxytocin's role in eating disorders,there is a need for a comprehensive review to integrate findings across neurobiological, genetic, hormonal, and therapeutic dimensions. This scoping review synthesizes existing literature on OXT's role in EDs and proposes a new theoretical perspective based on diverse research findings.

Methods: In accordance with PRISMA guidelines, we systematically synthesized all peer-reviewed articles indexed on PubMed which focused on both OXT and EDs as of December 2023 (k = 32 studies, n = 1942 participants). After summarizing this literature in tables, we completed the narrative synthesis with a discussion of mechanisms informed by an unstructured literature review.

Results: The existing studies propose a connection between OXT receptor Oxtr polymorphisms and ED diagnoses, severity of symptoms, macronutrient preferences, reward function, and early life stress. In addition, OXT plasma levels normalized with ED symptom reduction. Although some OXT studies have failed to show therapeutic changes in food intake and weight, few have reported ameliorations in brain function, food-related attentional bias, cognition, and emotional regulation. Some data have also suggested a contributory role of the transforming growth factor β (TGFβ) and sterol regulatory element binding proteins (SREBPs) to the etiology of EDs through Oxtr expression.

Conclusion: Although the current evidence does not support OXT as a standalone cause of or treatment for EDs, OXT research holds promise as a way of identifying future therapies, and OXT itself may serve as a valuable adjunct.

Rising evidence suggests that Metabolic Syndrome (MetS) would be correlated with the development of neurodegenerative diseases. Although this has emerged as a relevant area of research, it has not been fully explored. It is not clear if a greater impairment of the metabolic peripheral environment is accompanied by a greater impairment of the central nervous system. We have previously shown that feeding rats with a high-sucrose diet (HSD) represents an animal model that resembles the human MetS phenotype. The aim of the present work was to assess in rats fed a HSD for a short (3 weeks-wk) or a long (15 weeks-wk) term, whether the worsening of the peripheral metabolic and hormonal profile that occur as the time of HSD consumption increases, is also accompanied by a worsening of oxidative stress in the cerebral cortex and/or cognitive behavior. Male Wistar rats received a HSD or a control diet during 3 wk or 15 wk. We found an increase in reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS), advanced glycation end products (AGEs) and glutathione peroxidase (GPx) and glutathione reductase (GR) enzyme activities in the cerebral cortex of 3 wk HSD-fed rats. All of these parameters, except for the GPx, were also increased in the 15 wk HSD-fed group and values were similar to those observed at 3 wk. Glutathione reduced form (GSH), catalase (CAT) activity and brain-to-body weight ratio were reduced in 15 wk HSD-fed animals. Glutathione S- transferase (GST) was similar in all dietary groups. A poor performance in novel object recognition test and T-maze memory tasks was observed in 3 wk and 15 wk HSD-fed rats in a similar magnitude. Our results add new evidence related to the association between an adverse peripheral metabolic environment and brain/cognitive dysfunction.

Natural rewards like regular sucrose consumption can buffer physiological and behavioral stress responses, likely mediated, at least in part, by increased plasticity in parvalbumin-positive (PV+) interneurons in the basolateral amygdala (BLA). As PV+ interneuron plasticity is tightly regulated by specialized extracellular matrix structures called perineuronal nets (PNNs), this study investigated the impact of regular sucrose consumption vs. repetitive stress on the PNNs that surround PV+ interneurons in the BLA, as well as the number of glutamatergic (vGLUT1) and GABAergic (vGAT) appositions that PV+ cells receive. Male rats were given an established limited sucrose intake (LSI) feeding paradigm (vs. water-fed controls) and were co-exposed to a brief restraint stress (vs. no stress controls), daily for 14 days. Sucrose consumption increased the proportion of PV+ cells that were surrounded by PNNs, independent of stress exposure. PV+ cells with PNNs had more vGLUT1-positive and fewer vGAT-positive appositions compared to those lacking PNNs. Additionally, sucrose consumption increased the ratio of excitatory/inhibitory appositions onto PV+ cells, suggesting the possibility of elevated PV+ interneuron tone, leading to greater inhibition of the BLA's stress-excitatory output. These findings indicate that sucrose consumption influences PNN formation and structural plasticity on PV+ interneurons in the BLA, which has implications for understanding the neurological mechanisms underlying stress resilience by natural rewards.

Objective: Chronic methamphetamine use is frequently associated with impairments in the attentional network (alerting, orienting, conflict networks) and related brain regions, which significantly trigger METH-related cravings. The aim of this study is to investigate the effects of moderate-intensity acute aerobic exercise on cravings and attentional networks in individuals with methamphetamine use disorders (MUD).

Methods: Using a cross-over design, this study recruited 32 male MUDs to randomly complete a 30min moderate-intensity aerobics exercise condition (65%-75% HRmax) and an assigned material reading control condition, with a 7-day washout interval. All participants completed Visual Analog Scales before, during, and after exercise, until the HR dropped to 110% of the resting heart rate, in preparation for the Attention Network Test (ANT).

Results: The aerobic exercise significantly reduces the participants' cravings. There were no differences observed in the efficiency of alerting and orienting networks between the aerobic exercise and control conditions, however, the efficiency of conflict network was enhanced after exercise. Furthermore, the results showed a significant negative correlation between the enhancements in conflict network efficiency and the reductions in post-exercise craving scores for both conditions.

Conclusion: Moderate-intensity acute aerobic exercise significantly improves the attentional network, especially enhancing the conflict network in individuals with MUD. Additionally, the improvement of the conflict network is closely related to the reduction in cravings in individuals with MUD, suggesting that aerobic exercise may reduce cravings through improvements in cognitive function.

Objectives: Multiple sclerosis (MS) is a chronic neurological disorder characterized by demyelination and neurodegeneration, leading to various physical, cognitive, and emotional challenges. Dual-task (DT) training, involving performing mental and physical tasks simultaneously, addresses the complex interaction between motor and cognitive functions.

Purpose: Given the extensive physical, cognitive, and mood-related issues in this population, this study aimed to examine the effects of combined aerobic-cognitive training (Brythonic) and aerobic training on brain-derived neurotrophic factor (BDNF), DT performance, and mood state in MS patients.

Methods: Thirty patients (22 women and 8 men) with relapsing-remitting multiple sclerosis (RRMS) and an expanded disability status scale (EDSS) score below four were randomly assigned to three groups: aerobic-cognitive training (Brythonic), aerobic training, and control. The training groups participated in 10 weeks of home-based online training, with two sessions per week. Each session included a 10-minute warmup, 15 to 35 min of exercise, and a 5-minute cool-down. The Brythonic group performed aerobic movements while reciting motivational words, forming a complete positive sentence over ten weeks. The aerobic group performed the same movements without cognitive tasks. Serum BDNF levels, DT performance, and profile of mood states (POMS) were measured before and after the 10-week training period. A two-way ANOVA with repeated measures was used to analyze differences between and within groups, with a significance level of P ≤ 0.05.

Results: BDNF levels significantly increased in the Brythonic group (P = 0.048) and significantly decreased in the control group compared to baseline. In the DT test, the Brythonic group showed significant improvements in the number of correct answers and DT values compared to the aerobic and control groups. The Brythonic group also had a significantly reduced response time compared to the control group. Additionally, selective speed significantly increased in both training groups. In the POMS test, the Brythonic group showed significant improvements in all items except depression compared to the control group. Within the Brythonic group, all items significantly improved from baseline.

Conclusion: This study demonstrated that combining motivational words with aerobic movements significantly impacts BDNF levels, DT performance, and mood states. Adding mental exertion to physical activity appears beneficial for patients with MS. Future studies should re-examine these findings with a larger patient cohort.

Background and aims: The glucose-centric hypothesis postulates that glycemic control may influence cognition. While research has examined the effects of breaking up sitting on blood glucose and inhibitory control, few studies have integrated these data and employed event-related potential (ERP) measures to delve into the neuroelectric processes. This study aimed to investigate the effects of breaking up sitting on postprandial blood glucose response, inhibitory control, and P3 component.

Methods: Eighteen healthy male participants [25 ± 4 years, 23.5 ± 3.2 kg/m² (mean ± SD)] were subjected to 3.5 h uninterrupted sitting (SIT) or with 3 min walking at 6.4 km/h every 30 min (ACTIVE) trials in a randomized crossover design. The Stroop task was administered to assess inhibitory control before and after SIT and ACTIVE trials, and electroencephalography was employed to derive stimulus-elicited P3 component. Finger prick blood glucose levels were collected at baseline, 0.5 h, 1 h, and 3.5 h during the trials.

Results: While no significant differences were found in inhibitory control performances between trials, greater P3 amplitude was found in the ACTIVE trial relative to the SIT trial (p = .041). Lower postprandial blood glucose iAUC was found in ACTIVE trial compared to SIT trial (p = .028), and this was correlated with the elevation of P3 amplitude (r = - 0.521, p = .023).

Conclusion: Breaking up sitting acutely facilitates neuroelectric indices of attentional processing, which is associated with the optimal postprandial blood glucose control.