Neuroscience
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Acute peripheral vestibular dysfunction is associated with a variety of postural and balance disturbances. Vestibular rehabilitation training (VRT) is widely acknowledged as an effective intervention for promoting vestibular compensation. Nevertheless, the broader implementation of early VRT is hindered by an incomplete understanding of its neurobiological mechanisms. ⋯ Our findings suggest that VRT facilitates the recovery of postural motor deficits during vestibular compensation, likely mediated by cell proliferation and glial responses, particularly the proliferation of microglia, in the MVN. Furthermore, we demonstrate that ultra-early rehabilitation training yields greater benefits for the long-term recovery of dynamic deficits following UVN. These results carry significant implications for the clinical implementation of early VRT in patients experiencing acute peripheral vestibular dysfunction.
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Major depressive disorder (MDD) is a complex neuropsychiatric disorder potentially influenced by factors such as stress and inflammation. Chronic stress can lead to maladaptive brain changes that may trigger immune hyperactivation, contributing to MDD's pathogenesis. While the involvement of inflammation in MDD is well established, the effects of inflammatory preconditioning in animals subsequently exposed to chronic stress remain unclear. ⋯ A trend toward elevated IL-17 levels was also observed at the peripheral level. These findings indicate that inflammatory preconditioning contributes significantly to behaviors phenotypically associated with MDD. Furthermore, the study suggests that these behavioral changes are linked to a dysfunctional immune response and impaired neuroplasticity.
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The experiment was designed to explore the effects and mechanism of Dilong on alleviating cyclophosphamide (CTX)-induced brain injury in mice. Fifty male SPF Kunming mice aged 6-8 weeks were randomly divided into five groups: Group A served as the control group; Group B received intraperitoneal injection of CTX; Groups C, D, and E were administered Dilong at doses of 100, 200, and 400 mg/kg respectively for 14 days after intraperitoneal injection of CTX. Results showed that after modeling, the movement speed of mice significantly decreased (P < 0.05), and the number of neurons in the hippocampus and cortex decreased. ⋯ Dilong significantly increased mitochondrial respiratory enzyme activity (P < 0.05), and the mitochondrial structure was restored to some extent. By significantly reducing NLRP3/TLR4/caspase1/pro caspase1/GSDMD (P < 0.05), it increased neuronal cell survival. This resulted in an increase in neuronal cell survival, thus exerting a protective effect on the brain.
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Estrogens and progesterone can have rapid effects on neuronal function and can modify the use of spatial navigation strategies dependent upon the prefrontal cortex, striatum, and hippocampus. Here, we assessed the effects of 17β-estradiol (E2), progesterone, and its metabolite allopregnanolone, on evoked excitatory postsynaptic potentials in the infralimbic region of the female rat prefrontal cortex. Field excitatory postsynaptic potentials (fEPSPs) evoked by stimulation of layer I were first characterized by recording responses at multiple depths between the cortical surface and the underlying white matter. ⋯ The effects of progesterone were not blocked by the nuclear progesterone receptor antagonist RU486 (1 µM). Both progesterone and allopregnanolone are known to activate membrane progesterone receptors, and we found that the membrane progesterone receptor agonist Org OD 02-0 facilitated EPSPs, and also occluded further increases induced by either progesterone or allopregnanolone. These results provide evidence that both progesterone and allopregnanolone facilitate synaptic responses in layer I of the infralimbic cortex by activating membrane progesterone receptors.