Physiology & Behavior最新文献

Food addiction (FA) is a complex clinical condition that refers to addiction to highly palatable foods, represented by compulsive eating behavior and an incapacity to control food consumption, similar to other forms of addiction. This review examines the literature on FA and its impact on eating disorders and obesity. Using databases such as PubMed, Cochrane Library and Google Scholar, recent studies were analyzed to show how FA may reduce treatment effectiveness, increase symptom severity, promote resistance to nutritional or pharmacological interventions, and elevate the risk of relapse. The search strategy used the keywords food addiction, obesity, eating disorders, psychotherapy, and dietary therapy, limiting the reference period to studies published in the last five years. In reviewing the available articles, several nuances emerged that are fundamental to understanding FA, including neurobiological mechanisms, psychiatric comorbidities, environmental determinants, alterations in the gut microbiota, and the pervasive influence of ultra-processed foods. Taken together, the data indicate that FA not only intensifies symptom manifestation but also contributes to worse outcomes, with reduced compliance to standard treatments and an increased likelihood of relapse. These observations underscore the importance of recognizing FA as a critical component in clinical practice; neglecting its role and symptom may compromise therapeutic efficacy. Further research is needed to establish integrative treatment models that include FA as a fundamental component of clinical patient care.

It remains unclear whether acute aerobic exercise can effectively mitigate the inhibitory control deficits caused by test anxiety. This study investigated the effects of 30 min of moderate-intensity acute aerobic exercise on inhibitory control and related neural activities in individuals with high test anxiety. Forty participants were randomly assigned to an aerobic exercise group or a seated-reading control group, completing pre- and post-intervention assessments spaced one week apart. Statistical analyses using a series of repeated-measures ANOVAs revealed that, compared to the control group, the exercise group showed a significant reduction in self-reported test anxiety. Behaviorally, exercise led to significantly faster reaction times across both congruent and incongruent trials, coupled with a specific reduction in the Flanker conflict effect (RT difference between conditions), indicating enhanced interference control. Electrophysiologically, analysis of event-related potentials demonstrated that acute exercise modulated key cognitive components: N2 amplitude was significantly reduced and P3 amplitude was significantly enhanced in both task conditions following exercise, with no comparable changes in the control group. These findings suggest that acute aerobic exercise can enhance inhibitory control and alleviate test anxiety in university students.

The present study aimed to determine whether apelin-13 facilitates lordosis behavior through the activation of specific hypothalamic kinases and to identify which signaling pathways mediate this response. Because lordosis is a well-established neuroendocrine indicator of female sexual receptivity, it served as an appropriate behavioral model to detect peptide-induced facilitation. Thus, we examined the role of protein kinase A (PKA), protein kinase C (PKC), mitogen activated protein kinase (MAPK), or Src kinase (Src), in the facilitation of lordosis behavior following bilateral intrahypothalamic injection of 0.75 μg of apelin-13 to ovariectomized-estradiol benzoate (OVX-EB) primed rats. Apelin-13 consistently induced lordosis at 30, 120, and 240 minutes post-infusion. To explore the role of these kinases, various inhibitors or their vehicles were administered bilaterally into the ventromedial hypothalamus (VMH) of OVX-EB-primed rats 30 min before the infusion of apelin-13. The inhibitors used were Rp-cAMPS for PKA, bisindolilmaleimide (BIS) for PKC, PD98059 for MAPK, and PP2 for Src. The VMH injection of Rp-cAMPS failed to reverse the facilitation of lordosis at the different times tested, while BIS or PP2 decreased the lordosis quotient (LQ) significantly only at 240 min without any statistical effect on the lordosis score (LS). However, PD98059 significantly reduced both the LQ and LS at 120 and 240 min. These data indicate that apelin-13 exerts its facilitatory effects on lordosis through MAPK, PKC, and/or Src, but not PKA pathways.

Sleep deprivation negatively impacts both physical and psychological health in both humans and animal models. Exercise, on the other hand, can have beneficial effects on various aspects of physical and mental health. However, little is known about the ways in which sleep deprivation and exercise may interact, especially for exceptionally high levels of exercise. We studied High Runner (HR) mice from a long-term artificial selection experiment to investigate how genetically high exercise level could impact the response to sleep deprivation. A total of 192 adult mice from four replicate HR and four non-selected Control lines (balanced for sex) completed six days of baseline wheel access, followed by three days with or without 6 h/day of total sleep deprivation (TSD) via gentle handling. As expected, HR mice ran farther and faster compared to Controls during days 1-6. TSD reduced the running distance and duration in mice from Control lines, while HR increased running speed and maintained distance (treatment × linetype interaction). TSD-induced changes in body mass differed between linetypes (treatment × linetype interaction): Controls tended to gain mass, whereas HRs lost mass. During the three days prior to TSD, HR mice consistently exhibited more active and fewer maintenance behaviors than Controls. TSD increased resting and decreased wheel activity in Controls but not HRs (treatment × linetype effects significant for both categories). These results demonstrate that genetically based high voluntary activity levels are associated with altered responses to TSD.