Neuroscience
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A decline in mitochondrial functions associated with ageing is the key factor of free radical generation which contributes to age-related pathologies. Protecting healthy functional mitochondrial networks with antioxidants is critical in promoting healthy ageing. This study aimed to investigate the protective effect of ergothioneine (EGT)-rich Lentinula edodes extract (LE-ETH) against tert-butyl hydroperoxide (t-BHP) assaulted senescent HT22 cells. ⋯ A total of 23 compounds consisting of phenols, fatty acids, and sterols were identified in the ethanolic extract. Pentanoic acid was the major compound identified in LE-ETH. These findings demonstrated that EGT-rich L.edodes mushroom is a potential neuroprotective agent which could serve as a potential therapeutic strategy for the preservation of mitochondrial functions in healthy ageing explorations.
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The trigeminal ganglion (TG) comprises primary sensory neurons responsible for orofacial sensations, subsequently projecting to the trigeminal nuclei in the brainstem. However, the circuit basis of nasal mechanosensation is not well characterized. Here we elucidate the anatomical organization of both peripheral and central projections of the TG. ⋯ In contrast, the MrgprD+ neurons only densely project to outer edge of Sp5C. In addition, we further determined the ascending pathway of the TG neurons. Taken together, our study demonstrates the peripheral and central projection pattern of mechanosensory neurons in the TG, which provides a basis for the future functional studies.
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Increasing evidence indicates that neuropeptide FF (NPFF) produces analgesic effects and augments opioid-induced analgesia at the spinal level. However, our recent research demonstrated that NPFF exerted complex opioid-modulating effects in an inflammatory pain model after intrathecal (i.t.) injection. Consistent with previous findings, we found that i.t. ⋯ Moreover, these modulating effects of spinal NPFFR2 were selectively targeting mu-opioid receptor, had no effect on delta- and kappa-opioid receptor agonist-induced analgesia. Finally, the opioid-modulating effects of NPFF were further verified using in vitro calcium imaging assay, demonstrating that pretreated with NPFF in primary-cultured spinal neurons significantly attenuated the inhibitory effects of morphine on high-K+-induced neuronal excitability. Taken together, our results suggested that NPFF exhibited dual modulating effects on morphine-induced analgesia after i.t. administration, which provides a possible mechanism to explain the complex opioid-modulating effects of endogenous NPFF systems.
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The most characteristic feature of the human electroencephalogram is the peak alpha frequency (PAF). While PAF has been proposed as a biomarker in several diseases and disorders, the disease mechanisms modulating PAF, as well as its physiological substrates, remain elusive. This has partly been due to challenges related to experimental manipulation and invasive procedures in human neuroscience, as well as the scarcity of animal models where PAF is consistently present in resting-state. ⋯ Using this conservative threshold, PAF was present in 18/20 pigs with a normal distribution of the peak frequency between 8-12 Hz, producing similar findings to human recordings. We show that PAF was present in 69.6 % of epochs of approximately six-minute-long resting-state recordings. In sum, we propose that the pig is a suitable candidate for investigating the neural mechanisms of PAF as a biomarker for disease and disorders such as pain, neuropsychiatric disorders, and response to pharmacotherapy.
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Ginsenoside Rg1 (Rg1) has been shown to treat a variety of human diseases, including Alzheimer's disease (AD). However, its mechanism in AD needs further investigation. Microglial cells (BV2) were treated with Aβ1-42 to induce AD cell models. ⋯ GATA4 interacted with PDE4A, and GATA4 facilitated Aβ1-42-induced BV2 cell injury by increasing PDE4A expression. Besides, GATA4 knockdown reduced PDE4A protein expression and inactivated PI3K/AKT axis, while these effects were abolished by PDE4A overexpression. In conclusion, our data suggested that Ginsenoside Rg1 inhibited microglial cell apoptosis and inflammation to attenuate AD progression by regulating the GATA4/PDE4A/PI3K/AKT axis.