Neuroreport
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Neuron-glial-related cell adhesion molecule (NrCAM) is a neuronal cell adhesion molecule that has been shown to be involved in several cellular processes in the peripheral nervous system, including neurite outgrowth. We recently reported that alternative splicing of Nrcam mRNA at exon 10 in the dorsal root ganglion (DRG) contributes to the peripheral mechanism of neuropathic pain. Specially, Nrcam antisense oligonucleotides (ASO) targeting Nrcam exon 10, attenuated neuropathic pain hypersensitivities in mice. ⋯ By immunostaining DRG neurons with different DRG markers, Nrcam ASO significantly reduced neurite lengths in neurofilament 200-, calcitonin gene-related peptide and isolectin B4-positive neurons in primary DRG neuronal culture. Moreover, Nrcam ASO activates epidermal growth factor receptor, which may mediate the effect of Nrcam ASO on neurite outgrowth of cultured DRG neurons. These results provide evidence that Nrcam ASO suppresses neurite outgrowth in DRG neurons by regulating alternative splicing of Nrcam gene at exon 10 and activation of epidermal growth factor receptor signaling, indicating the differential roles of NrCAM variants/isoforms in neurite outgrowth.
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We previously showed differences in brain grey matter volume changes between patients with early-onset adult depression (EOD) and late-onset adult depression (LOD). Here, we aim to identify whether cortical thickness (CT) is affected by the age of onset in patients with depression. ⋯ MDD patients with different age at onset show distinct CT alterations, suggesting potentially divergent pathological mechanisms of EOD and LOD.
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This study was designed to determine the association between motor functional recovery and interhemispheric imbalance in cortical brain activity in sub-cortical stroke patients with moderate-to-severe upper limb hemiparesis admitted to the convalescent rehabilitation ward. ⋯ Our results suggested that activation of the non-lesional hemisphere in sub-acute stroke associated with motor recovery in moderate-to-severe upper limb hemiparesis. A multidisciplinary rehabilitation of stroke patients with moderate-to-severe upper limb hemiparesis might enhance the compensatory movements and pre-existing motor network from the non-lesional motor cortex.
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Remote ischemia preconditioning (RIPC) is a convenient and effective method for alleviating cerebral ischemia-reperfusion injury (CIRI). However, to date, the underlying mechanism has not been fully elucidated. The aim of this research was to explore the protective mechanism of RIPC on the brain after CIRI. ⋯ The inflammatory response and apoptosis are two important processes involved in brain dysfunction after CIRI. The JAK2/STAT3 signaling pathway has an underlying relationship with these two processes. These findings suggest that RIPC can alleviate the damage to brain tissue by CIRI by regulating the JAK2/STAT3 signaling pathway negatively.
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Although it has been shown that sevoflurane exposure could impair the cognitive function, there are few effective treatments to prevent this disorder. Suberoylanilide hydroxamic acid (SAHA), an inhibitor of histone deacetylase, plays an important role in hippocampal memory formation, which has been proven to enhance memory. As such, we explored whether SAHA could improve the memory impairment induced by sevoflurane in adult mice. ⋯ SAHA also significantly reversed the decreases in Ac-H3, brain-derived neurotrophic factor, tropomyosin-related kinase B, and p-cAMP response element-binding expressions induced by sevoflurane exposure, and reduced the level of apoptosis-related protein cleaved caspase-3. We concluded that cognitive and synaptic plasticity impairments induced by sevoflurane exposure could be reversed by normalizing the histone acetylation state. The effect is related to inhibiting cell apoptosis and activating the brain-derived neurotrophic factor/tropomyosin-related kinase B/cAMP response element-binding signaling pathway in the hippocampus.