Neuroscience
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Age-related hearing loss in humans has been associated with cognitive decline, though the underlying mechanisms remain unknown. We investigated the long-term effects of hearing loss on attention, impulse control, social interaction, and neural activity within medial prefrontal cortex (mPFC) subregions. Hearing loss was induced in adult rats via intracochlear neomycin injection (n = 13), with non-operated rats as controls (n = 10). ⋯ Electrophysiology showed decreased power in theta, alpha, and beta frequency, and enhanced high gamma band in the mPFC in deafened rats, which was most pronounced in the cingulate subregion (Cg1). The number of NeuN+ and Parvalbumin+ cells, however, did not differ between groups. The behavioral deficits together with the altered neuronal activity found in the Cg1 subregion of the mPFC in adult deafened rats may be used as an endophenotype to elucidate the mechanisms behind the cognitive decline seen in older patients with hearing loss.
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Neuropeptide-S (NPS) has been demonstrated to mitigate learning and memory deficits in experimental models of Parkinson's Disease (PD). Despite this, the precise mechanisms through which NPS exerts its influence on cognitive functions remain to be fully unknown. This study aims to elucidate the effects of central administration of NPS on learning and memory deficits associated with an experimental rat hemiparkinsonian model, examining both electrophysiological and molecular parameters. ⋯ In 6-OHDA-lesioned rats, NPS treatment significantly (p < 0.05) enhanced the amplitude of LTP at the dentate gyrus/perforant path synapses. Furthermore, NPS significantly (p < 0.05) increased the number of pCaMKII and GluR1 immunoreactive cells in the hippocampus, which had been diminished due to 6-OHDA, except for GluR2 levels. These findings provide insight into the mechanisms by which central NPS administration enhances cognitive functions in an experimental model of PD, highlighting its potential therapeutic benefits for addressing cognitive deficits in PD.
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The adverse impact of disturbmitochondrialbiogenesis onearly brain injury (EBI) following subarachnoid haemorrhage (SAH) has been broadly recognized and is closely associated with oxidative stress and neuronal apoptosis. Previous studies have indicated the therapeutic potential of Ropinirole, a dopamine D2 agonist, in Ischemic Stroke. However, there is a lack of evidence regarding the ability of Ropinirole to enhance mitochondrial biogenesis and quality control after subarachnoid haemorrhage. ⋯ Further research showed that, Ropinirole therapy inhibit Drp1-mediated fission by accelerating the activity of fusion protein Mfn2/OPA1 along with regulating the translocation of PGC1-α and SIRT3 through restricting cytochrome C inside mitochondria to maintain mitochondrial metabolism. Ropinirole exerted neuroprotective effects by improving mitochondrial activity in a PGC1-α/SIRT3-dependent way via regulating Drp1 mediated fission. The effective treatment for SAH-induced EBI may involve increasing biogenesis and inhibiting excessive mitochondrial fission with Ropinirole.
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Pain and itch are unpleasant and distinct sensations that give rise to behaviors such as reflexive withdrawal and scratching in humans and mice. Interestingly, it has been observed that pain modulates itch through the neural circuits housed in the brain and spinal cord. However, we have yet to fully understand the identities and mechanisms by which specific neural circuits mediate pain-induced modulation of itch. ⋯ The RVMTacr1 neurons were found to be nociceptive, sufficient for inhibiting itch, and necessary for pain-induced itch suppression. Moreover, through brain-wide anterograde and retrograde viral tracing studies, we found that the RVMTacr1 neurons are bidirectionally connected with LPBN, periaqueductal gray (PAG), and lateral hypothalamic area (LHA). Thus, together, our data indicate that the RVMTacr1 neurons integrate nociceptive information to mediate itch-induced scratching and can mediate the physiological effects of itch through their downstream targets.
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Astragaloside Ⅳ (AS-Ⅳ) improved the motor behavior of Parkinson's disease (PD) mouse but the alteration of imaging in the PD mice brain was unclear. PD models were established by unilateral injection of rotenone (ROT) into the substantia nigra pars compacta (SNc) of mice. AS-Ⅳ (20 mg/kg) was intraperitoneally injected once daily for 14 days. ⋯ After administering AS-Ⅳ, bilateral SN fractional anisotropy (FA) values increased, whereas mean diffusivity (MD) values decreased in mice, according to the diffusion tensor imaging (DTI) analysis. In addition, AS-Ⅳ treatment significantly reduced the T2 values of the T2-mapping. In summary, AS-Ⅳ improved motor impairments and efficiently performed neuroprotective functions in the ROT-induced mouse model.