Neuroscience
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Noise-induced hidden hearing loss (NIHHL), one of the family of conditions described as noise-induced hearing loss (NIHL), is characterized by synaptopathy following moderate noise exposure that causes only temporary threshold elevation. Long noncoding RNAs (lncRNAs) mediate several essential regulatory functions in a wide range of biological processes and diseases, but their roles in NIHHL remain largely unknown. In order to determine the potential roles of these lncRNAs in the pathogenesis of NIHHL, we first evaluated their expression in NIHHL mice model and mapped possible regulatory functions and targets using RNA-sequencing (RNA-seq). ⋯ KEGG analysis was also used to identify the potential pathways being affected in NIHHL. These analyses allowed us to identify the guanine nucleotide binding protein alpha stimulating (GNAS) gene as a key transcription factor and the adrenergic signaling pathway as a key pathway in the regulation of NIHHL pathogenesis. Our study is the first, to our knowledge, to isolate a lncRNA mediated regulatory pathway associated with NIHHL pathogenesis; these observations may provide fresh insight into the pathogenesis of NIHHL and may pave the way for therapeutic intervention in the future.
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Valproic acid (VPA) administered to mice during the early postnatal period causes social, cognitive, and motor deficits similar to those observed in humans with autism spectrum disorder (ASD). However, previous studies on the effects of early exposure to VPA have largely focused on behavioral deficits occurring before or during the juvenile period of life. Given that ASD is a life-long condition, the present study ought to extend our understanding of the behavioral profile following early postnatal VPA into adulthood. ⋯ This may indicate a disinhibited or impulsive phenotype in male, but not female, mice treated with VPA during the second week of postnatal life. Decreased dendritic spine density and dendritic spine morphological abnormalities in the mPFC of VPA-treated mice may be indicative of PFC hypofunction, consistent with the observed behavioral differences. Since these types of long-lasting deficits are not exclusively found in ASD, early life exposure to VPA may reflect dysfunction of a neurobiological domain common to several developmental disorders, including ASD, ADHD, and conduct disorder.
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Demyelination significantly affects brain function. Several experimental methods, each inducing varying levels of myelin and neuronal damage, have been developed to understand the process of myelin loss and to find new therapies to promote remyelination. The present work investigates the effect of one such method, lysolecithin administration, on the white matter tracts in the olfactory system. ⋯ While both the LOT and AC exhibited significant demyelination at 7 dpi and had returned to control levels by 30 dpi, the process differed between the two tracts. Remyelination occurred more rapidly in the LOT: substantial recovery was observed in the LOT by 14 dpi, but not in the AC until 21 dpi. The findings indicate that (a) the LOT and AC are indeed suitable tracts for studying lysolecithin-induced de- and remyelination and (b) experimental demyelination proceeds differently between the two tracts.
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Little is known about the neural mechanisms that mediate differential action-selection responses to communication and echolocation calls in bats. For example, in the big brown bat, frequency modulated (FM) food-claiming communication calls closely resemble FM echolocation calls, which guide social and orienting behaviors, respectively. ⋯ We combined information obtained from spike number and spike triggered averages (STA) to reveal a robust classification of neuron selectivity for communication or echolocation calls. These data highlight the importance of temporal acoustic structure for differentiating echolocation and food-claiming social calls and point to general mechanisms of natural sound processing across species.
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Recently, alterations of complexity due to brain disorders have been demonstrated using brain entropy (BEN), while the changes of brain complexity in stroke, a common cerebrovascular disease, remain unclear. In this research, resting-state functional magnetic resonance imaging (fMRI) was performed to explore the alterations of brain complexity using BEN in twenty stroke patients with motor deficits and nineteen matched healthy controls. The sample entropy (SampEn) was applied to build the BEN mapping for each participant. ⋯ Moreover, significantly positive correlations between BEN values and Fugl-Meyer Assessment scores were detected in the ipsilesional SFGdor and ipsilesional SMA. Mutual information independence was observed between BEN and regional homogeneity (ReHo), amplitude of low-frequency fluctuations (ALFF), respectively, in the stroke patients. Our findings implied that brain complexity had been impacted after stroke, and also suggested that BEN could be a complementary tool for evaluating the motor impairment after stroke.