Neuroscience
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Proprioception is somatic sensation that allows us to sense and recognize position, posture, and their changes in our body parts. It pertains directly to oneself and may contribute to bodily awareness. Likewise, one's face is a symbol of oneself, so that visual self-face recognition directly contributes to the awareness of self as distinct from others. ⋯ We examined whether the self-face recognition and the proprioceptive illusion commonly activated the inferior fronto-parietal cortices connected by the SLF III in a right-hemispheric dominant manner. Despite the difference in sensory modality and in the body parts involved in the two tasks, both tasks activated the right inferior fronto-parietal cortices, which are likely connected by the SLF III, in a right-side dominant manner. Here we discuss possible roles for right inferior fronto-parietal activity in bodily awareness and self-awareness.
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Microglia are immune cells in the brain and play a pivotal role in the progression of ischemic injury, but the gene expression and signaling pathways related to the activation of microglia following ischemia remain unclear. In our experiment, we used digital gene expression (DGE) analysis to profile the transcriptome of ischemic tissue in a photothrombosis model. DGE analysis identified that a total of 749 genes were differentially regulated (643 up-regulated and 106 down-regulated) after 2days and 7days following stroke. ⋯ DGE analysis indicated that specific genes related to microgliosis were regulated after ischemia. Consistent with the changes in transcriptome, the results from histological analysis of transgenic mice revealed that the microglia proliferated and aggregated surrounding the ischemic core during the period from 2days to 7days following photothrombosis. Together, these results suggested that transcriptomic changes in microglial genes after stroke may have a profound implication for pathophysiology and treatment of stroke.
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Chronic intermittent exposure to ethanol (EtOH; CIE) that produces binge-like levels of intoxication has been associated with age-dependent deficits in cognitive functioning. Male Sprague-Dawley rats were exposed to CIE (5g/kg, 25% EtOH, 13 intragastric gavages) beginning at three ages: early adolescence (postnatal day [PD] 28), mid-adolescence (PD35) and adulthood (PD72). In experiment 1, rats were behaviorally tested following CIE. ⋯ Following recovery, neurotrophin levels in all CIE rats recovered. Our results indicate that intermittent binge-like EtOH exposure leads to acute disruptions in FC BDNF levels and long-lasting behavioral deficits. However, the type of cognitive impairment and its duration differ depending on the age of exposure.
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The simple cells of the visual cortex respond over a narrow range of stimulus orientations, and this tuning is invariant to the contrast at which the stimulus is presented. The inputs to a single cell derive from a population of thalamic cells that provide a bell-shaped tuning width and offset that increases with stimulus contrast. Synaptic depression, noise and inhibition have been proposed as feedforward mechanisms to explain why these increases do not appear in simple cells. ⋯ Thalamocortical synaptic depression could only be used to counteract a small fraction of the offset otherwise the relationship between contrast and response rate was disrupted. Only broadly tuned simple and complex cell inhibition could counteract the remaining offset for all stimulus contrasts but complex cell inhibition reduced the gain of the response. These results suggest unequal contributions of these feedforward mechanisms with thalamic synaptic noise widening tuning widths for low contrasts, synaptic depression counteracting a small component of the offset and synaptic inhibition completely removing the remaining offset to produce contrast-invariant orientation tuning.
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Social bonds, especially attachment relationships, are crucial to our health and happiness. However, what we know about the neural substrates of these bonds is almost exclusively limited to rodent models and correlational experiments in humans. Here, we used socially monogamous non-human primates, titi monkeys (Callicebus cupreus) to experimentally examine changes in regional and global cerebral glucose metabolism (GCGM) during the formation and maintenance of pair bonds. ⋯ In contrast, control areas changed only marginally more than GCGM. These findings confirm the large effects of social bonds on GCGM. They also suggest that more studies should examine how social manipulations affect whole-brain FDG uptake, as opposed to assuming that it does not change across condition.