Neuroscience
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Hypnosis is a psychological technology proved to be effective in respiratory motion control, which is essential to reduce radiation dose during radiotherapy. This study explored the neural mechanisms and cognitive neuroscience of hypnosis for respiration control by functional magnetic resonance imaging with a within-subject design of 15 healthy volunteers in rest state (RS) and hypnosis state (HS). Temporal fluctuation and signal synchronization of brain activity were employed to investigate the altered physiological performance in hypnosis. ⋯ Compared to RS, enhanced positive correlations were observed between temporal fluctuation and signal synchronization in HS. Most importantly, coupled correlation was observed between temporal fluctuation and global signal synchronization within the identified intrinsic networks (R = 0.3843, p > 0.05 in RS; R = 0.6212, p < 0.005 in HS). The findings provide implications for the neural basis of hypnosis for respiratory motion control and suggest the involvement of emotional processing and regulation of perceptual consciousness in hypnosis.
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Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) have been implicated in the trafficking of postsynaptic glutamate receptors, including N-methyl-d-aspartate (NMDA)-subtype glutamate receptors (NMDARs) that are critical for nociceptive plasticity and behavioral sensitization. However, the components of SNAREs complex involved in spinal nociceptive processing remain largely unknown. Here we found that SNAP25, syntaxin4, VAMP2 and Munc18-1 were localized at postsynaptic sites and formed the complex in the superficial lamina of spinal cord dorsal horn of rats. ⋯ Disruption of the molecular interaction between SNAP25 with its SNARE partners by using a blocking peptide derived from the C-terminus of SNAP25 effectively repressed the surface and synaptic accumulation of GluN2B-containing NMDARs in CFA-injected rats. This peptide also alleviated inflammatory mechanical allodynia and thermal hypersensitivity. These data suggested that SNAREs complex assembly in spinal cord dorsal horn was involved in the inflammatory pain hypersensitivity through promoting NMDAR synaptic trafficking.
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C1q/TNF-related protein 4 (CTRP4) has been reported to decrease food intake and regulate energy homeostasis. However, its underlying mechanism and signaling pathway remain unknown. Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and signal transducer and activator of transcription 3 (STAT3) signaling pathway in normal chow-fed mice. ⋯ The changes of neuropeptides were accompanied by significant increased STAT3 phosphorylation and decreased SOCS3 levels. The same changes of neuropeptides and STAT3 signaling were also found in N2a cells after CTRP4 overexpression intervention. Collectively, our data reveals that CTRP4 induces the activation of STAT3 signaling and decreases food intake.
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Lysosomal network dysfunction is a prominent feature of Alzheimer's disease (AD). Although transgenic mouse models of AD are known to model some aspects of lysosomal network dysfunction, the lysosomal network has not yet been examined in the knock-in AppNL-G-F/NL-G-F mouse. We aimed to determine whether AppNL-G-F/NL-G-F mice exhibit disruptions to the lysosomal network in the brain. ⋯ AppNL-G-F/NL-G-F mice also exhibited elevated activity of β-hexosaminidase and cathepsins D/E and elevated levels of selected lysosomal network proteins, namely LAMP1, cathepsin D and microtubule-associated protein light chain 3 (LC3-II) in the cerebral cortex, as determined by western blot. Elevation of cathepsin D did not change the extent of co-localisation between cathepsin D and LAMP1 in the AppNL-G-F/NL-G-F mice. These findings demonstrate that perturbations of the lysosomal network occur in the AppNL-G-F/NL-G-F mouse model, further validating its use an animal model of pre-symptomatic AD.
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Myelinated Ah-type vagal ganglion neurons (VGNs) were specific subpopulation in adult females, rather than neonate and key players in sexual dimorphism in baroreflex afferent function and closely associated with estrogen. However, the gender related development changes in Ah-type VGNs remains unknown. To quantify the developmental changes in ion channels overtime, the whole-cell patch-clamp technique was performed and three afferent fiber types of VGNs were identified upon electrophysiological/pharmacological validations. ⋯ The coordinated changes in the current density of certain ion channels may be the underlying mechanism of developmental changes in AP waveform and neuroexcitability. As expected, the coordinated change between the down-regulation of iberiotoxin-sensitive and up-regulation of 4-aminopyridine-sensitive K+ currents played a key role in shaping AP and neuroexcitability in Ah-types during development. Our results demonstrated that the myelinated Ah-type VGNs in males almost disappear at 4 weeks old where closes to adult and the correlative ion channel changes contribute to the sexual dimorphism in visceral afferent function.