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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In the adult hippocampal dentate gyrus (DG), the majority of newly generated cells are eliminated by apoptotic mechanisms. The apoptosis repressor with caspase recruitment domain (ARC), encoded by the Nol3 gene, is a potent and multifunctional death repressor that inhibits both death receptor and mitochondrial apoptotic signaling. The aim of the present study was to parse the role of ARC in the development of new granule cell neurons. ⋯ ARC knockout is not associated with increased numbers of microglia or with microglia activation. However, hippocampal brain-derived neurotrophic factor (BDNF) protein content is significantly increased in ARC-/- mice, possibly representing a compensatory response. Collectively, our results suggest that ARC plays a critical cell-autonomous role in preventing cell death during adult granule cell neogenesis.
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The great majority of neurons in the superficial dorsal horn of the spinal cord are excitatory interneurons, and these are required for the normal perception of pain and itch. We have previously identified 5 largely non-overlapping populations among these cells, based on the expression of four different neuropeptides (cholecystokinin, neurotensin, neurokinin B and substance P) and of green fluorescent protein driven by the promoter for gastrin-releasing peptide (GRP) in a transgenic mouse line. Another peptide (neuropeptide FF, NPFF) has been identified among the excitatory neurons, and here we have used an antibody against the NPFF precursor (pro-NPFF) and a probe that recognises Npff mRNA to identify and characterise these cells. ⋯ By examining phosphorylation of extracellular signal-regulated kinases, we show that the NPFF cells can respond to different types of noxious and pruritic stimulus. Ablation of somatostatin-expressing dorsal horn neurons has been shown to result in a dramatic reduction in mechanical pain sensitivity, while somatostatin released from these neurons is thought to contribute to itch. Since the great majority of the NPFF cells co-expressed somatostatin, these cells may play a role in the perception of pain and itch.