Neuroscience
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This study aimed to explore the neural mechanisms underlying food decision making in unsuccessful restrained eaters (US-REs) and successful restrained eaters (S-REs). During a functional magnetic resonance imaging scan, participants were required to choose between pairs of high- and low-calorie foods under the following conditions: the congruent condition (choose between high- and low-calorie foods with the same level of tastiness) and incongruent condition (choose between high-calorie foods tastier than the corresponding low-calorie foods). Subsequently, the participants' diets were monitored for one week. ⋯ Our results suggest that US-REs have a strong reward response to food. Compared to US-REs, S-REs are more guided more by the goal of weight control, and exhibit strong functional connections between the conflict-monitoring and inhibitory-control regions. Therefore, eating enjoyment and weight-control goals influence restrained eating in daily life.
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Physical activity (PA) has been shown to benefit various cognitive functions and promote neuroplasticity. Whereas the effects of PA on brain anatomy and function have been well documented in older individuals, data are scarce in young adults. Whether high levels of cardiorespiratory fitness (CRF) achieved through regular PA are associated with significant structural and functional changes in this age group remains largely unknown. ⋯ Transcranial magnetic stimulation (TMS) revealed higher corticospinal excitability in high- compared to low-fit individuals reflected by greater input/output curve amplitude and slope. No group differences were found for other TMS (short-interval intracortical inhibition and intracortical facilitation), diffusion MRI (fractional anisotropy and apparent fiber density), structural MRI (cortical thickness) and magnetic resonance spectroscopy (NAA, GABA, Glx) measures. Taken together, the present data suggest that brain changes associated with increased CRF are relatively limited, at least in primary motor cortex, in contrast to what has been observed in older adults.
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Transcranial static magnetic stimulation (tSMS) is known to influence behavioral and neural activities. However, although the left and right dorsolateral prefrontal cortex (DLPFC) are associated with different cognitive functions, there remains a lack of knowledge on a difference in the effects of tSMS on cognitive performance and related brain activity between left and right DLPFC stimulations. To address this knowledge gap, we examined how differently tSMS over the left and right DLPFC altered working memory performance and electroencephalographic oscillatory responses using a 2-back task, in which subjects monitor a sequence of stimuli and decide whether a presented stimulus matches the stimulus presented two trials previously. ⋯ Our preliminary results revealed that while tSMS over the left and right DLPFC impaired working memory performance to a similar extent, the impacts of tSMS on brain oscillatory responses were different between the left and right DLPFC stimulations. Specifically, tSMS over the left DLPFC increased the event-related synchronization in beta band whereas tSMS over the right DLPFC did not show such an effect. These findings support evidence that the left and right DLPFC play different roles in working memory and suggest that the neural mechanism underlying the impairment of working memory by tSMS can be different between left and right DLPFC stimulations.
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Previous studies revealed that high long-term hypothalamic-pituitaryadrenal (HPA) axis activity measured by the hair cortisol concentrations predicts lower acute stress cortisol response and reported the influences of hair cortisol on brain activity during acute stress exposure. However, considering that long-term HPA axis activity has a close relationship with the brain's resting-state functional connectivity (RSFC), the current study aimed to explore the role of RSFC between limbic and salience network in this relationship. Seventy-seven healthy participants underwent resting-state imaging scans before performing the acute ScanSTRESS task. ⋯ Moreover, high HairE levels were significantly correlated with enhanced RSFC between limbic and salience networks, while RSFC was negatively associated with acute stress cortisol response. Importantly, the RSFC between left insula and left parahippocampus mediated the association between HairE and acute cortisol stress response. Taken together, this study uncovers the important role of RSFC between salience and limbic networks in the long-term relationship between HairE and acute cortisol response and contributes to a deeper understanding of the individual differences in acute stress response.
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Melatonin supplementation has been shown to delay age-related hearing loss (ARHL) progression. Previously, melatonin was found to inhibit neuronal mitochondrial DNA (mtDNA) release, as well as inhibit cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling, thereby delaying the onset of central nervous system diseases. Therefore, we hypothesized that melatonin may delay the progression of hearing loss in the C57BL/6J presbycusis mouse model by inhibiting cGAS-STING signaling in the auditory pathway. ⋯ We found that the 12-month-old control mice exhibited significant hearing loss, increased cytosolic mtDNA, increased expression of inflammatory factors TNF-α, IL-6, IFN-β, Cxcl10, and Ifit3, up-regulated cGAS and STING expression, and enhanced interferon regulatory factor 3 (IRF3) phosphorylation in the C57BL/6J mouse cochlea, inferior colliculus, and auditory cortex. Melatonin treatment significantly improved hearing, decreased cytosolic mtDNA, suppressed the expression of inflammatory cytokines TNF-α, IL-6, IFN-β, Ifit3, and Cxcl10, down-regulated cGAS and STING expression, and attenuated IRF3 phosphorylation in the C57BL/6J mouse cochlea, inferior colliculus, and auditory cortex. This study suggested that melatonin had a protective effect on auditory function in the C57BL/6J presbycusis mouse model, which may be mediated through reducing mtDNA release, inhibiting the cGAS-STING signaling pathway in the auditory pathway.