Neuroscience
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Visceral pain in inflammatory and functional gastrointestinal conditions is a major clinical problem. The exact mechanisms underlying the development of pain, during and after visceral inflammation are unknown. However, clinical and pre-clinical evidence suggests plasticity within the spinal cord dorsal horn is a contributing factor. ⋯ Conversely, several measures of intrinsic excitability were altered in a manner that would decrease SDH network excitability following colitis. We propose that during inflammation, sensitization of colonic afferents results in increased signaling to the SDH. This is accompanied by plasticity in SDH neurons whereby their intrinsic properties are changed to compensate for altered afferent activity.
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Trauma and tumor compressing the brain distort underlying cortical neurons. Compressed cortical neurons remodel their dendrites instantly. The effects on axons however remain unclear. ⋯ However, KLC and KHC expressions in the cell bodies of the layer II/III pyramidal neurons partially recovered. Our results show cerebral compression compromised cortical axonal outputs and reduced transcallosal projection. Some of these changes did not recover in long-term decompression.
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Although deep-brain stimulation (DBS) of the lateral habenula (LHb) has been successfully applied to treatment-resistant depression for years, the mechanism is still unclear. Previous researches have demonstrated that LHb-DBS elevates brain monoamine neurotransmitters. However, these changes do not account for the treatment efficacy on treatment-resistant depression, or the rapid behavioral effects in rats; the evidence suggests that altered synaptic potentiation may contribute to the treatment effects. ⋯ These effects were blocked by the L-type voltage-dependent calcium channel (L-VDCC) antagonist, nifedipine. Furthermore, in vitro LHb-DBS increased both the frequency and width of spontaneous spikes generated by CA1 pyramidal neurons, which contribute to Ca2+ influx through L-VDCC. Our findings suggest that L-VDCC-mediated synaptic potentiation underlies the antidepressant effects of LHb-DBS, and suggest that astrocytic regulation of Ca2+ influx and associated synaptic changes maybe novel targets for developing antidepressant treatments.
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Neuregulin-1β (NRG-1β) has great potential to be developed into therapeutics for neuroprotection. The aim of the current study was to analyze the effects and possible signaling pathway of NRG-1β on brain tissues in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). ⋯ NRG-1β exerts a neuroprotective effect through the JNK signaling pathway in MCAO/R rats.
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Sestrin 2 (SESN2) is a stress-inducible protein that protects tissues from oxidative stress and delays the aging process. However, its role in maintaining the functional and structural integrity of the cochlea is largely unknown. Here, we report the expression of SESN2 protein in the sensory epithelium, particularly in hair cells. ⋯ Hair cell death occurred by caspase-8 mediated apoptosis. Compared to C57BL/6J control mice, Sesn2 KO mice displayed enhanced expression of proinflammatory genes and activation of basilar membrane macrophages, suggesting that loss of SESN2 function provokes the immune response. Together, these results suggest that Sesn2 plays an important role in cochlear homeostasis and immune responses to stress.