Neuroscience
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Electroencephalogram (EEG)-based quantitative pain measurement is valuable in the field of clinical pain treatment, providing objective pain intensity assessment especially for nonverbal patients who are unable to self-report. At present, a key challenge in modeling pain events from EEG is to find invariant representations for intra- and inter-subject variations, where current methods based on hand-crafted features cannot provide satisfactory results. Hence, we propose a novel method based on deep learning to learn such invariant representations from multi-channel EEG signals and demonstrate its great advantages in EEG-based pain classification tasks. ⋯ The proposed method aims to jointly preserve the spatial-spectral-temporal structures of EEG, for learning representations with high robustness against intra-subject and inter-subject variations, making it more conducive to multi-class and subject-independent scenarios. Empirical evaluation on 4-level pain intensity assessment within the subject-independent scenario demonstrated significant improvement over baseline and state-of-the-art methods in this field. Our approach applies deep neural networks (DNNs) to pain intensity assessment for the first time and demonstrates its potential advantages in modeling pain events from EEG.
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Fragmentation of the daily sleep-wake rhythm with increased nighttime awakenings and more daytime naps is correlated with the risk of development of Alzheimer's disease (AD). To explore whether a causal relationship underlies this correlation, the present study tested the hypothesis that chronic fragmentation of the daily sleep-wake rhythm stimulates brain amyloid-beta (Aβ) levels and neuroinflammation in the 3xTg-AD mouse model of AD. Female 3xTg-AD mice were allowed to sleep undisturbed or were subjected to chronic sleep fragmentation consisting of four daily sessions of enforced wakefulness (one hour each) evenly distributed during the light phase, five days a week for four weeks. ⋯ Sleep fragmentation also stimulated neuroinflammation as shown by increased expression of markers of microglial activation and proinflammatory cytokines measured by q-RT-PCR analysis of hippocampal samples. No significant effects of sleep fragmentation on Aβ, tau, or neuroinflammation were observed in the cerebral cortex. These studies support the concept that improving sleep consolidation in individuals at risk for AD may be beneficial for slowing the onset or progression of this devastating neurodegenerative disease.
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Orexin-producing cells in the lateral hypothalamic area have been shown to be involved in a wide variety of behavioral and cognitive functions, including the recall of appetitive associations and a variety of social behaviors. Here, we investigated the role of orexin in the acquisition and recall of socially transmitted food preferences in the rat. Rats were euthanized following either acquisition, short-term recall, or long-term recall of a socially transmitted food preference and their brains were processed for orexin-A and c-Fos expression. ⋯ In the infralimbic cortex, we found that social behavior was significantly predictive of c-Fos expression, with social behaviors related to olfactory exploration appearing to be particularly influential. We additionally found that appetitive behavior was significantly predictive of orexin-A activity in a sex-dependent matter, with the total amount eaten correlating negatively with orexin-A/c-Fos colocalization in male rats but not female rats. These findings suggest a potential sex-specific role for the orexin system in balancing the stimulation of feeding behavior with the sleep/wake cycle.
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Microglia serve as resident immune cells in the brain, responding to insults and pathological developments. They have also been implicated in shaping synaptic development and regulation. The present study examined microglial cell density in a number of brain regions across select postnatal (P) ages along with the effects of valproic acid (VPA) on microglia density. ⋯ Finally, animals treated with VPA at P60 exhibited decreased microglia density in the hippocampus only. These results suggest rapid VPA-induced increases in microglial cell density in a developmentally-regulated fashion which differs across distinct brain areas. Furthermore, in the context of prior reports that early VPA causes excitotoxic damage, the present findings suggest early VPA exposure may provide a model for studying altered microglial responses to early toxicant challenge.
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Presbycusis, or age-related hearing loss (ARHL), is primarily associated with sensory or transduction nerve cell degeneration in the peripheral and/or central auditory systems. During aging, the auditory system shows mitochondrial dysfunction and increased inflammatory responses. Mitochondrial dysfunction promotes leakage of mitochondrial DNA (mtDNA) into the cytosol, which activates the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway to induce type I interferon and inflammatory responses. ⋯ The results showed that cGAS-positive immunoreactive cells were observed in the cochlea, inferior colliculus, and auditory cortex. Levels of cytosolic mtDNA, cGAS, STING, phosphorylated interferon regulatory factor 3, and cytokines were significantly increased in the cochlea, inferior colliculus, and auditory cortex of 6-, 9-, and 12-month-old mice compared with 3-month-old mice. These findings suggested that cytosolic mtDNA may play an important role in the pathogenesis of ARHL by activating cGAS-STING-mediated type I interferon and inflammatory responses.