Neuroscience
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Intracranial hypertension (IH) is a medical or surgical emergency that can be the common ending of various neurological disorders, such as traumatic brain injury, cerebral vascular diseases and brain tumors. However, the molecular mechanisms underlying IH-induced neuronal apoptosis have not been fully determined, and the treatments are symptomatic, insufficient and complicated by side-effects. In this study, a cellular model induced by compressed gas treatment in primary cultured rat cortical neurons was performed to mimic IH-induced neuronal injury in vitro. ⋯ Furthermore, the results using inhibitors of each signaling pathway demonstrated that ROS mediated the compression-induced ER stress and mitochondrial dysfunction in cortical neurons. In conclusion, our results demonstrated that compression induced apoptosis in primary cultured cortical neurons, which was associated with ROS mediated ER stress and mitochondrial dysfunction. Pharmacological compounds or agents targeting mitochondrial dysfunction and ER stress associated oxidative stress might be ideal candidates for the treatment of IH-related neurological diseases.
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Diabetes is a chronic degenerative disease that represent a major threat to public health worldwide. Once the disease is established, one of the major concerns about the diabetes complications is the development of neuropathy. This study established an experimental model that evaluates the effect of type 1 diabetes on nociceptive challenges in the temporomandibular joint (TMJ). ⋯ Diabetic animals pre-treated with Protein Kinase C (PKC)-α and -β inhibitor (GO6976) or PKC-β inhibitor (LY333531) significantly increased capsaicin-induced nociception in the TMJ higher protein levels of Na+/K+-ATPase pump in the trigeminal ganglia. On the other hand, although diabetes inhibits formalin-induced nociception higher protein levels of pro-inflammatory cytokine IL1-β and chemokine CINC-1/CXCL-1 were observed. Overall, the results of the present work suggest that diabetes causes a hyporesponsiveness of C-fiber and a potentialization of the inflammatory response which may result in the degenerative process of periarticular tissues without pain perception.
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The influence of neuroinflammation in the development and progression of Parkinson's disease (PD) remains unknown. Macrophage migration inhibitory factor (MIF) is a multipotent and key cytokine involved in the pathogenesis of acute and chronic inflammatory and immune disorders. The aim of this study was to investigate the neuroprotective effects mediated by MIF in PD. ⋯ Upregulating MIF expression resulted in a higher concentration of LC3B-II than the control group (P < 0.001). Finally, LC3 puncta were markedly increased in the MIF upregulated group and in the MIF + MPP+ group. This study indicates that MIF mediates a neuroprotective effect via suppressing inflammatory responses, inhibiting apoptosis and inducing autophagy in PD.
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Turning elicits Freezing of Gait (FoG) episodes in people with Parkinson's disease (PD) and is thought to require higher cortical control compared to straight ahead gait. Functional near infrared spectroscopy (fNIRS) has been used to examine prefrontal cortex (PFC) activity while walking, but the relationship between PFC activity and turn performance remains unclear. The aim of this pilot study was to examine PFC activity during turning in PD and healthy controls, and to investigate the association between PFC activity and turning. ⋯ In addition, higher PFC is associated with worse FoG in PD + FoG (r = 0.57, p = .048) and with lower number of turns in PD - FoG (r = -0.70, p = .002). The increased PFC activity in PD and the association between higher PFC activity and poorer turning performance may be a sign of poor movement automaticity in PD. Although further investigations are required, these pilot findings may guide development of personalized treatments to improve motor automaticity in PD.
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Humans can recognize living organisms and understand their actions solely on the basis of a small animated set of well-positioned points of light, i.e. by recognizing biological motion. Our aim was to determine whether this type of recognition and integration also occurs during the perception of one's own movements. The participants (60 females) were immersed with a virtual reality headset in a virtual environment, either dark or illuminated, in which they could see a humanoid avatar from a first-person perspective. ⋯ Kinesthetic illusions also occurred with point-light avatars, albeit less frequently and a little less intense, and only when the visual environment was optimal for slow motion detection of the point-light display (lit environment). We conclude that kinesthesia does not require visual access to an elaborate representation of a body segment. Access to biological movement can be sufficient.