Neuroscience
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Autism is a developmental disorder defined by the presence of a triad of communication, social and stereo typical behavioral characteristics with onset before 3years of age. In spite of the fact that there are potential environmental factors for autistic behavior, the dysfunction of serotonin during early development of the brain could be playing a role in this prevalence rise. Serotonin can modulate a number of developmental events, including cell division, neuronal migration, cell differentiation and synaptogenesis. ⋯ However, hyposerotonemia may be also relevant to the development of sensory as well as motor and cognitive faculties. And the paucity of placenta-derived serotonin should have potential importance when the pathogenesis of autism is considered. This review briefly summarized the developmental disruptions of serotonin signaling involved in the pathogenesis of autism during early development of the brain.
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In stroke-prone spontaneously hypertensive rats (SHRSP/Izm), ischemia induces swelling of astrocytes, a process that subsequently leads to neuronal death. Following ischemic insult, arginine vasopressin (AVP) can induce edema and l-serine released by astrocytes supports the survival of neuronal cells. The purpose of this study was to examine whether AVP contributed to the regulation of l-serine production following ischemic stroke. ⋯ AVP-mediated enhanced expression of ASCT1 was blocked by the addition of bumetanide. These results suggest that the AVP-mediated attenuated expression of ASCT1 in astrocytes is associated with reduced l-serine production in SHRSP/Izm astrocytes. We hypothesize that reduction of gene expression by AVP might be related to the induction of stroke in the SHRpch1_18 rat strain.
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The atrial volume receptor reflex arc serves to regulate plasma volume. Atrial volume receptors located in the endocardium of the atrial wall undergo mechanical deformation as blood is returned to the atria of the heart. The mechanosensitive channel(s) responsible for regulating plasma volume remain to be determined. ⋯ The small conductance Ca(2+)-activated K(+) channels (SK2 and SK4) were also present, however there was no relationship between SK and TRP channels. SK2 channels were expressed in nerves in the epicardium, while SK4 channels were in some regions of the endocardium but appeared to be present in epithelial cells rather than sensory endings. In conclusion, we have provided the first evidence for TRPC1 and TRPV4 channels as potential contributors to mechanosensation in the atrial volume receptors.
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In seeking evidence for the presence and characteristic range of coupled time scale(s) of putative implicit turbulent attractors of dorsal frontal lobe magnetic fields, the recorded nonstationary, nonlinear MEG signals were non-orthogonally decomposed using Huang's Empirical Mode Decomposition, EMD, (Huang and Attoh-Okine, 2005) into 16 Intrinsic Mode Functions, EMD→IMFi, i=1…16. Measures known to be invariant in non-uniformly hyperbolic (turbulent) dynamical systems, topological entropy, hT, metric entropy, hM, non-uniform entropy, hU and power spectral scaling exponent, α, were imposed on each of the IMFi which evidenced most clearly an invariant temporal scale zone of IMFi, i=6…11, for hT, which we have found to be the most robust of invariant measures of MEG's magnetic field turbulent attractors (Mandell et al., 2011a,b; Mandell, 2013). The ergodic theory of dynamical systems (Walters, 1982; Pollicott and Yuri, 1998) allows the inference that an implicit attractor with consistently hT>0 will also evidence at least one positive Lyapounov exponent indicating the presence of a turbulent attractor with exponential separation of nearby initial conditions, exponential convergence of distant points and disordering, mixing, of orbital sequences. It appears that this approach permits the inference of the presence of chaotic, turbulent attractor and its characteristic time scales without the invocation of arbitrary n-dimensional embedding, phase space reconstructions or (inappropriate) orthogonal decompositions.
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Curculigoside A may be a powerful way of protecting the brain against a wide variety of injury. In the present study, we sought to elucidate whether Curculigoside A contributes to induce angiogenesis and its mechanisms. To this end, we examined the role of Curculigoside A on proliferation, invasion, and tube formation in the human brain microvascular endothelial cell line (HBMEC) in vitro. ⋯ VEGF expression was increased by Curculigoside A and counteracted by the soluble VEGF receptor 1 (sFlt-1, VEGF antagonist) and KG-501 in HMBEC. Tube formation was enhanced by Curculigoside A and counteracted by VEGF receptor blocker-SU1498, KG-501 and Egr-3 siRNA. It may be suggested that Curculigoside A induces angiogenesis in vitro via a programed VCAM-1/Egr-3/CREB/VEGF signaling axis.