Neuroscience
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Phox2a and Phox2b are two homeodomain transcription factors playing a pivotal role in the development of noradrenergic neurons during the embryonic period. However, their expression and function in adulthood remain to be elucidated. Using human postmortem brain tissues, rat stress models and cultured cells, this study aimed to examine the alteration of Phox2a and Phox2b expression. ⋯ Exposing SH-SY5Y cells to corticosterone significantly increased expression of Phox2a and Phox2b, which was blocked by corticosteroid receptor antagonists. Taken together, these experiments reveal that Phox2 genes are expressed throughout the lifetime in the LC of humans and Fischer 344 rats. Alterations in their expression may play a role in major depressive disorder and possibly other stress-related disorders through their modulatory effects on the noradrenergic phenotype.
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Diglossia in the Arabic language refers to the socio-linguistic situation in which Spoken Arabic (SA), which is the first to be acquired, is used for everyday communications, while Literary Arabic (LA), acquired at school for reading and writing, is also used for formal functions. Although some authors consider SA and LA as a first and second language, the question of how these are managed in the brain has not yet been understood. Using functional magnetic resonance brain imaging (fMRI) analysis, this study aimed at exploring the neural basis of diglossia during picture naming in two contexts. ⋯ Behavioral analysis showed that naming in SA was slightly easier than LA and considerably easier than Hebrew. fMRI analysis showed no difference between SA and LA. Hebrew compared to SA revealed activation differences explainable in terms of engagement of language control modules and second- to first-language effects. These findings, discussed in the light of previous findings in bilingual literature, support the view that dominance in diglossia is modality-dependent.
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The vestibular system enables humans to estimate self-motion, stabilize gaze and maintain posture, but these behaviors are impacted by neural noise at all levels of processing (e.g., sensory, central, motor). Despite its essential importance, the behavioral impact of noise in human vestibular pathways is not completely understood. Here, we characterize the vestibular imprecision that results from neural noise by measuring trial-to-trial vestibulo-ocular reflex (VOR) variability and perceptual just-noticeable differences (JNDs) in the same human subjects as a function of stimulus intensity. ⋯ VOR and perceptual imprecision both increased with stimulus intensity and were broadly similar over a range of stimulus velocities, consistent with a common noise source that affects motor and perceptual pathways. This contrasts with differing perceptual and motor stimulus-dependent imprecision in visual studies. Either stimulus-dependent noise or non-linear signal processing could explain our results, but we argue that afferent non-linearities alone are unlikely to be the source of the observed behavioral stimulus-dependent imprecision.
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The present study set out to assess the possible role of the medial prefrontal cortex (mPFC) cannabinoid CB1 receptors and BDNF/cFOS signaling pathways in morphine-dextromethorphan (DXM) cross state-dependent memory (SDM) using male Wistar rats. Changes on the levels of BDNF and cFOS proteins in the PFC were examined by Western blot analysis. Present results revealed that levels of BDNF and cFOS proteins were significantly increased in the animals that were trained in the passive avoidance apparatus. ⋯ Interestingly, pre-test intra-mPFC injections of ACPA inhibited cross-SDM between the drugs which was associated with an elevation of BDNF expression in the PFC. Additionally, pre-test administration of an ineffective dose of DXM (10 mg/kg, i.p.) could not reverse morphine-induced memory loss, while pre-test intra-mPFC injections of AM-251 potentiated morphine-DXM cross-SDM. Taken together, it can be concluded that mPFC through CB1cannabinoid receptors has a critical role in morphine-DXM cross-SDM which may be associated with the PFC BDNF/cFOS signaling pathway.
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Brain damage is a leading cause of death in patients with cardiac arrest (CA). The accumulation of succinate during ischemia by succinate dehydrogenase (SDH) is an important mechanism of ischemia-reperfusion injury. It was unclear whether inhibiting the oxidation of accumulated succinate could also mitigate brain damage after CA. ⋯ Western blotting analysis showed that DMM inhibited the activation of caspase-3 and enhanced the expression of HIF-1α. Moreover, DMM inhibited excessive hyperpolarization of MMP after CPR, and prevented the release of cytochrome C. Therefore, inhibiting SDH by DMM alleviated brain damage after CA, and the main mechanisms included inhibiting the excessive hyperpolarization of MMP, reducing the generation of mtROS and stabilizing the structure of HIF-1α.