Neuroscience
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Non-synaptic transmission is pervasive throughout the nervous system. It appears especially prevalent in peripheral ganglia, where non-synaptic interactions between neighboring cell bodies have been described in both physiological and pathological conditions, a phenomenon referred to as cross-depolarization (CD) and thought to play a role in sensory processing and chronic pain. CD has been proposed to be mediated by a chemical agent, but its identity has remained elusive. ⋯ Furthermore, we show that DRG glial cells also play a cell-type specific role in CD regulation. Fluorocitrate-induced glial inactivation had no effect on A-cells but enhanced CD in C-cells. These findings shed light on the mechanism of CD in the DRG and pave the way for further analysis of non-synaptic neuronal communication in sensory ganglia.
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Schwann cells (SCs) combined with acellular nerve allografts (ANAs) effectively promote the regeneration and repair of peripheral nerves, but the exact mechanism has not been fully elucidated. However, the disadvantages of SCs include their limited source and slow rate of expansion in vitro. Previous studies have found that adipose-derived stem cells have the ability to differentiate into Schwann-like cells. ⋯ The results showed that adipose-derived Schwann-like cells combined with ANAs markedly promoted sciatic nerve regeneration and repair. These findings also demonstrated that the expression of neurotrophic factors (NFs) was increased, and the expression of Janus activated kinase2 (JAK2)/P-JAK2, signal transducer and activator of transcription-3 (STAT3)/P-STAT3 was decreased in the spinal cord after SNI. Therefore, these results suggested that highly expressed NFs in the spinal cord could promote nerve regeneration and repair by inhibiting activation of the JAK2/STAT3 signaling pathway.
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Although the neural basis underlying visuospatial reasoning has been widely explored by neuroimaging techniques, the brain activation patterns during naturalistic visuospatial reasoning such as tangram remains unclear. In this study, the directional functional connectivity of fronto-parietal networks during the tangram task was carefully inspected by using combined functional near-infrared spectroscopy (fNIRS) and conditional Granger causality analysis (GCA). Meanwhile, the causal networks during the traditional spatial reasoning task were also characterized to exhibit the differences with those during the tangram task. ⋯ Further correlation analyses showed that the behavioral performance in the spatial reasoning rather than the tangram task manifested the relationship with the connectivity between the frontal and parietal cortex. Our findings demonstrate that the tangram task measures a different aspect of the visuospatial reasoning ability which requires more trial-and-error strategies and creative thinking rather than inductive reasoning. In particular, the frontal cortex is mostly involved in tangram puzzle-solving, whereas the interaction between frontal and parietal cortices is regulated by the hands-on experience during the tangram task.
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An important pathology in Parkinson's disease (PD) is the earlier and more severe degeneration of noradrenergic neurons in the locus coeruleus (LC) than dopaminergic neurons in the substantia nigra. However, the basis of such selective vulnerability to insults remains obscure. Using noradrenergic and dopaminergic cell lines, as well as primary neuronal cultures from rat LC and ventral mesencephalon (VM), the present study compared oxidative DNA damage response markers after exposure of these cells to hydrogen peroxide (H2O2). ⋯ Consistent with these measurements, exposure of SK-N-BE(2)-M17 cells to H2O2 resulted in higher levels of reactive oxygen species (ROS). Further experiments showed that exposure of SK-N-BE(2)-M17 cells to H2O2 caused an increased level of noradrenergic transporter, reduced protein levels of copper transporter (Ctr1) and 8-oxoGua DNA glycosylase, as well as amplified levels of Cav1.2 and Cav1.3 expression. Taken together, these experiments indicated that noradrenergic neuronal cells seem to be more vulnerable to oxidative damage than dopaminergic neurons, which may be related to the intrinsic characteristics of noradrenergic neuronal cells.
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Noise-induced hearing loss generally induces loudness recruitment, but sometimes gives rise to hyperacusis, a debilitating condition in which moderate intensity sounds are perceived abnormally loud. In an attempt to develop an animal model of loudness hyperacusis, we exposed rats to a 16-20 kHz noise at 104 dB SPL for 12 weeks. Behavioral reaction time-intensity functions were used to assess loudness growth functions before, during and 2-months post-exposure. ⋯ Consistent with central gain models, the gross neural responses from the auditory cortex and amygdala were proportionately much larger than those from the cochlea. However, despite central amplification, the population responses in the auditory cortex and amygdala were still below the level needed to fully account for hyperacusis and/or recruitment. Having developed procedures that can consistently induce hyperacusis in rats, our results set the stage for future studies that seek to identify the neurobiological events that give rise to hyperacusis and to develop new therapies to treat this debilitating condition.