Neuroscience
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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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It is widely recognized that opening and closing the eyes can direct attention to external or internal stimuli processing. This has been confirmed by studies showing the effects of changes in visual stimulation changes on cerebral activity during different tasks, e.g., motor imagery and execution. However, an essential aspect of creating a mental representation of motion, such as imagery perspective, has not yet been investigated in the present context. ⋯ Furthermore, the stronger desynchronization of alpha rhythms from motor areas in the EO, than EC condition confirmed previous effects obtained during real movements. It was also found that simulating movement under EC/EO conditions affected signal classification accuracy, which has practical implications for MI-BCI effectiveness. These findings suggest that shifting processing toward external or internal stimuli modulates brain rhythm oscillations associated with different perspectives on the mental representation of movement.
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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.
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The blockade of 5-HT6 receptors represents an experimental approach that might ameliorate the memory deficits associated with brain disorders, including Alzheimer's disease and schizophrenia. However, the synaptic mechanism by which 5-HT6 receptors control the GABAergic and glutamatergic synaptic transmission is barely understood. ⋯ The effects of pharmacological manipulation of the 5-HT6 receptor were limited to GABAergic transmission and did not affect the strength of field excitatory postsynaptic potentials mediated by the Schaffer collaterals axons. Lastly, in a modified version of the Pavlovian autoshaping task that requires the activation of the hippocampal formation, we demonstrated that the anti-amnesic effect induced by the blockade of the 5-HT6 receptor is prevented when the GAT1 transporter is blocked, suggesting that modulation of GABAergic transmission is required for the anti-amnesic properties of 5-HT6 receptor antagonists.
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Previous study showed that electroacupuncture (EA) produced a protective effect on cerebral ischemia-reperfusion injury (CIRI) in rats and may correlate with the anti-inflammatory effects of microglia. This study aimed to investigate further whether EA could modulate neuroinflammation by targeting the Signal Transducer and Activator of Transcription 6 (STAT6) and Peroxisome Proliferator-Activated Receptor γ (PPARγ) pathway, the key regulator of microglia. Middle cerebral artery occlusion (MCAO) rats were used, and 6 h after reperfusion, EA interventions were performed in Chize (LU 5), Hegu (LI 4), Sanyinjiao (SP 6), and Zusanli (ST 36) on the affected side of the rats, the group that received EA + STAT6 phosphorylation inhibitor AS1517499 was used as a parallel control. ⋯ The data showed that EA significantly alleviated nerve injury, reduced infarct volume, enhanced the expression and activity of STAT6/PPARγ pathway, inhibited NF-κB activity, increased M2 microglia numbers and anti-inflammatory factor release, and inhibited microglia M1-type polarization and pro-inflammatory factor expression. In contrast, inhibition of STAT6 phosphorylation exacerbated neural damage, inhibited STAT6/PPARγ pathway activity, promoted microglia M1-type polarization and exacerbated neuroinflammation, resulting in an attenuated positive effect of EA intervention. Therefore, we concluded that EA intervention could attenuate microglia-associated neuroinflammation by enhancing the expression and activity of STAT6/PPARγ pathway, thereby reducing CIRI in MCAO rats.