Neuroscience
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Benzophenone-3 (BP-3) is the most commonly used UV filter in cosmetics, which is absorbed through the skin and crosses the blood-brain barrier. This compound increases extracellular glutamate concentrations, lipid peroxidation, the number of microglia cells and induces process of apoptosis. The aim of this study was to determine the effect of BP-3 on the activation and polarization of microglial cells in the frontal cortex and hippocampus of adult male rats exposed to BP-3 prenatally and then for two weeks in adulthood. ⋯ The in vitro study conducted in the primary culture of rat frontal cortical microglia cells showed that BP-3 increased the LPS-stimulated release of pro-inflammatory cytokines IL-1α, IL-1β, TNFα, but in cultures without LPS there was decreased IL-1α, IL-6 and TNFα production, while the IL-18 and IP-10 was elevated. The obtained results indicate that differences in the level of immunoactivation between the frontal cortex and the hippocampus may result from the action of this compound on glucocorticoid receptors. In turn, changes in cytokine production in microglial cells indicate that BP-3 aggravates the LPS-induced immunoactivation.
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Previous studies by us and others have shown that RING finger protein 213 (RNF213) is associated with cerebrovascular disease and systemic vasculopathy. Indeed, Rnf213 mRNA expression is increased in cerebral ischemia reperfusion injury (CIRI). The purpose of the present study was to investigate the role of Rnf213 in CIRI. ⋯ According to TTC staining and Bederson neurological scale, removal of Rnf213 decreased brain infarct volume and improved neurological deficit score, although the restoration of cerebral blood flow after MCAO was similar in WT and Rnf213-/- mice. In addition, the levels of p-Akt, p-GSK-3β, β-catenin and Bcl-2 were significantly increased 24 h after MCAO in the ischemic penumbra of the Rnf213-/- mice compared to WT mice, indicating that Rnf213 removal may ameliorate neuronal apoptosis by regulating the Akt/GSK-3β/β-catenin/Bcl-2 signaling pathway. Taken together, our study reveals that Rnf213 regulates neuronal apoptosis in CIRI, therefore impacting on brain infarct volume in brain ischemia.
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Organisms control their visual worlds by moving their eyes, heads, and bodies. This control of "gaze" or "looking" is key to survival and intelligence, but our investigation of the underlying neural mechanisms in natural conditions is hindered by technical limitations. Recent advances have enabled measurement of both brain and behavior in freely moving animals in complex environments, expanding on historical head-fixed laboratory investigations. ⋯ While the neural circuits for reflexive and voluntary gaze behaviors traverse somewhat independent brainstem and spinal cord circuits, both can be modulated by feedback, meaning that most gaze behaviors are learned rather than hardcoded. Despite this flexibility, there are broadly enumerable neural pathways commonly adopted among primate gaze systems. Parallel pathways which carry simultaneous evolutionary and homeostatic drives converge in superior colliculus, a layered midbrain structure which integrates and relays these volitional signals to brainstem gaze-control circuits.
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This study elucidates the neural mechanisms underlying increasing cognitive load while walking by employing 2 versions of a response inhibition task, the '1-back' version and the more cognitively demanding '2-back' version. By using the Mobile Brain/Body Imaging (MoBI) modality, electroencephalographic (EEG) activity, three-dimensional (3D) gait kinematics and task-related behavioral responses were collected while young adults (n = 61) performed either the 1-back or 2-back response inhibition task. Interestingly, increasing inhibitory difficulty from 1-back to 2-back during walking was not associated with any detectable costs in response accuracy, response speed, or gait consistency. ⋯ During hits, ERP changes were found over left-parietal regions during latencies related to orienting attention and subsequent selection and execution of the motor plan. The pattern of attenuation in walking-related EEG amplitude changes, during 2-back task performance, is thought to reflect more effortful recalibration of neural processes, a mechanism which might be a key driver of performance maintenance in the face of increased cognitive demands while walking. Overall, the present findings shed light on the extent of the neurocognitive capacity of young adults and may lead to a better understanding of how factors such as aging or neurological disorders could impinge on this capacity.
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Mental rotation is a core indicator of spatial ability, and a threshold for cognitive impairment may exist at approximately 4,000 m above sea level, but the specific thresholds for the severity of hypoxia in Tibetan indigenous populations in mental rotation ability remain largely unknown. To determine whether a threshold for mental rotation impairment exists in indigenous residents, we related a mental rotation task to inter-individual differences in a range of behavioral performance and neuropsychological characteristics across 51 indigenous Tibetan highlanders and 34 matched controls at three different altitudes (sea level, 2,900 m, and 4,200 m). Analyses of reaction time showed delayed behavioral responses in the 4,200 m altitude group. ⋯ Moreover, a time-frequency analysis showed significantly enhanced alpha- and beta-band power values for the 4,200 m altitude participants after stimulus presentation. The impairment in mental rotation ability is related to hypoxia and can be attributed to the absence of sufficient cognitive resources, which demonstrates the existence of a threshold for the effects of high altitude on the brain's mental rotation ability. Taken together, our findings have important implications for exploring the altitude threshold for the influence of high-altitude exposure on brain function, as well as for guiding the development of innovative strategies to optimize the response of the organism against chronic hypoxia-induced under extreme environments.