Neuroscience
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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.
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The glare illusion enhances the perceived brightness of a central white area surrounded by a luminance gradient, without any actual change in light intensity. In this study, we measured the varied brightness and neurophysiological responses of electroencephalography (EEG) and pupil size with the several luminance contrast patterns of the glare illusion to address the question of whether the illusory brightness changes to the glare illusion process in the early visual cortex. We hypothesized that if the illusory brightness enhancement was created in the early stages of visual processing, the neural response would be similar to how it processes an actual change in light intensity. ⋯ We found the SSVEP amplitude was lower in the glare illusion than in the control condition, especially under high luminance contrast conditions. Furthermore, we found the probable mechanisms of the inhibited SSVEP amplitude to the high luminance contrast of glare illusion based on the greater pupil constriction, thereby decreasing the amount of light entering the pupil. Thus, the brightness enhancement in the glare illusion is already represented at the primary stage of visual processing linked to the larger pupil constriction.
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Response inhibition - the suppression of prepotent behaviours when they are inappropriate - has been thought to rely on executive control. Against this received wisdom, it has been argued that external cues repeatedly associated with response inhibition can come to trigger response inhibition automatically without top-down command. The current project endeavoured to provide evidence for associatively-mediated motor inhibition. ⋯ Once trained, the subjects received transcranial magnetic stimulation applied over their primary motor cortex during passive observation of either the stop signal (i.e. without any need to stop a response) or an equally familiar control stimulus never associated with stopping. Analysis of motor-evoked potentials showed that corticospinal excitability was reduced during exposure to the stop signal, which likely involved stimulus-driven activation of intracortical GABAergic interneurons. This result provides evidence that, through associative learning, stop-associated stimuli can engage local inhibitory processes at the level of the motor cortex.
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Emotional Stability Interacts with Cortisol Levels before fMRI on Brain Processing of Fearful Faces.
Functional-Magnetic-Imaging (fMRI) is widely adopted to investigate neurophysiological correlates of emotion processing (EP). However, studies have reported that scanning procedures in neuroimaging protocols may increase or cause anxiety and psychological distress related with the scanning, thus inducing peripheral cortisol release. These phenomena may in turn impact on brain EP. ⋯ In the context of lower ES, the opposite Δc-brain activity relationship was found. Our results suggest that the stressful potential of fMRI interacts with personality traits in modulating brain activity during EP. These findings should be taken into account when interpreting neuroimaging studies especially exploring brain physiology during EP.
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Alzheimer's disease (AD) in the elderly is frequently accompanied by chronic cerebral hypoperfusion (CCH), which impairs the clearance of amyloid beta (Aβ) due to the dysfunction of the blood-brain barrier (BBB) and accelerates the AD pathology. Since the coagulation and complement cascades are associated with BBB dysfunction and AD pathology, we investigated the expression changes of coagulation (fibrinogen alpha chain-FGA, coagulation factor XIII A chain-Factor XIIIα) and complement (plasma protease C1 inhibitor-C1-INH, Complement component 3-C3) factors in the brain of novel AD model (APP23) mice with CCH at 12 months of age. Immunohistochemical and immunofluorescent analysis showed that the expressions of FGA, Factor XIIIα, C1-INH and C3 were significantly increased in cerebral neocortex, hippocampus, and thalamus of APP23 + CCH group (n = 12) as compared with wild type (WT, n = 10) and APP23 (n = 10) groups (⁎P < .05 and ⁎⁎P < .01 vs WT; #P < .05 and ##P < .01 vs APP23), especially near and inside of neurovascular unit. The present study suggests that CCH activated both the coagulation and complement cascades in a novel AD model mice brain accompanied by the acceleration of AD pathology.