Neuroscience
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We aimed to investigate the role of dorsal and ventral visual systems in rapid naming of simple Chinese characters. Twenty college students (10 female; Mage = 22.5 years) were required to covertly read a character- and a cross-matrix during an fMRI experiment. A basic prosaccade and a prosaccade-naming task were also performed to confirm the functional significance of the findings. ⋯ Moreover, in the character-matrix reading, we found a negative correlation between the reaction time of naming in the prosaccade-naming task and the EC strength from visual word form area to superior temporal gyrus and a positive correlation between the reaction time in the basic prosaccade task and the EC strength from middle frontal gyrus to intraparietal sulcus. The cross-matrix scanning did not show any brain-behavior relationship. These results suggest that while the dorsal visual system is mainly engaged in eye-movement control, the ventral system is associated more with orthographic processing and orthography-phonology mapping.
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The promotion of angiogenesis is a promising therapeutic strategy for ischemic stroke. Many long noncoding RNAs (lncRNAs) are related to angiogenesis following ischemic stroke. LncRNA small nucleolar RNA host gene 12 (SNHG12) was upregulated in oxygen-glucose deprivation (OGD)-exposed primary brain microvascular endothelial cells and in microvessel from middle cerebral artery occlusion (MCAO) animal brains. ⋯ Furthermore, we found that SNHG12 functioned as a competing endogenous RNA for miR-150 to regulate VEGF expression. Additionally, overexpression of SNHG12 improved the recovery of neurological function, reduced infarct volume and miR-150 expression, increased vascular density and VEGF expression in the infarct border zone of MCAO mice. In conclusion, SNHG12 promotes the angiogenesis following ischemic stroke via miR-150/VEGF pathway, which further clarified the mechanism of angiogenesis after ischemic stroke and provides a target for the treatment of this disease.
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Activation of the inflammasome complex contributes to the inflammatory response and cell death under pathologic conditions. The nucleotide-binding oligomerization domain-like receptor pyrin domain-containing 2 (NLRP2) inflammasome is activated in astrocytes after cerebral ischemia, which can aggravate ischemic damage. Apoptosis signal-regulating kinase 1 (ASK1) is an early activator and immune-regulator after ischemic injury, that can lead to cell death. ⋯ ASK1 silencing or inhibition efficiently reduced NLRP2 inflammasome components and pro-inflammatory cytokine levels in mice and cultured astrocytes. Our findings identify a key role for ASK1 in regulating astroglial inflammasomes after cerebral ischemia. We suggest ASK1 as one of the main targets for astroglial inflammasomes in ischemic stroke.
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Stress plays a pivotal role in the development and/or exacerbation of functional gastrointestinal (GI) disorders. The paraventricular nucleus of the hypothalamus (PVN) contains neurons that are part of the hypothalamic-pituitary-adrenal axis as well as preautonomic neurons innervating, among other areas, gastric-projecting preganglionic neurons of the dorsal vagal complex (DVC). The aim of the present study was to test the hypothesis that stress adaptation upregulates oxytocin (OXT) within PVN-brainstem vagal neurocircuitry. ⋯ Brainstem and hypothalamic nuclei were analyzed immunohistochemically for the presence of both OXT-immunopositive cells in identified preautonomic PVN neurons as well as OXT fibers in the DVC. Rats exposed to chronic homotypic, but not chronic heterotypic stress, had a significant increase in both number of CTB+ OXT co-localized neurons in the PVN as well as density of OXT-positive fibers in the DVC compared to control rats. These data suggest that preautonomic OXT PVN neurons and their projections to the DVC increase following adaptation to stress, and suggest that the possible up-regulation of OXT within PVN-brainstem vagal neurocircuitry may play a role in the adaptation of GI responses to stress.
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As one of the bisphosphonate derivatives, etidronate has proved to be beneficial to spatial learning and memory deficits caused by two-vessel occlusion (2-VO). In this study, the novel drug etidronate-zinc complex (Eti-Zn) was used to detect its role in synaptic plasticity and learning and memory functions in a rat model of 2-VO. Chronic cerebral hypoperfusion was induced by permanent occlusion of the common carotid artery bilaterally in adult Sprague-Dawley rats. ⋯ Moreover, Eti-Zn treatment reduced both the over-activation of microglia and the expressions of neuroinflammatory cytokines (TNF-α, IL-1β and IL-6) in the hippocampus. The increased NF-κB signaling pathway in the hippocampus of 2-VO rats was reversed after Eti-Zn treatment. In summary, these findings suggest that Eti-Zn could ameliorate the synaptic plasticity and cognitive impairments by reducing neuroinflammation in 2-VO model rats.