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Brain activity requires the regulation of excitatory and inhibitory neurons. GABAergic interneurons are considered to prevent hyperexcitability in brain. Severe GABAergic deficits have been proved to cause pathological hyperexcitability. Most cortical interneurons originate from the ventral telencephalon and then undergo a long tangential migration to the cortex, followed by radial migration into developing cortical plate. Among them, tangential migration is considered to be the main migration manner of interneurons. The process is rather complex but also precise. With the deepening research on the tangential migration of cortical neurons, many molecules have been proved to play important roles in the process of migration. In this review, we mainly describe the migration path and migration manner of interneurons, and its underlying mechanism in two aspects. On the one hand, neurotrophins such as BDNF, NT-4, GDNF, HGF and neurotransmitters such as GABA, Glu, DA can enhance the motility of interneurons. On the other hand, several protein families as well as proteoglycans, such as Ephrin, Sema and Nrg, can bind to membrane-bound or secreted guidance cues of interneurons, providing direction clues for neuronal migration. In this review, we discussed the tangential migration of interneurons in mice, in order to provide novel insights into the regulatory molecular mechanisms of cerebral cortical development and help to develop new targets against defects in neural developments.
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Autophagy represents one of the essential cellular mechanism to maintain homeostasis within cells, performing multiple biological functions during tumorigenesis. Base on the unique physicochemical properties of inorganic nanomaterials, supplemented by easy modification and targeting and so on, they could be used to regulate autophagy, controlling the occurrence and development of tumor and finally achieve treatment. This article primarily reviews the application of several representative inorganic nanomaterials, such as Gold nanoparticles, Silver nanoparticles, Iron oxide nanoparticles, Fullerene C60 nanomaterials, Graphene oxide nanomaterials in regulating autophagy of tumor cells and achieving treatment in recent years.
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<p><b>OBJECTIVE</b>To explore the effects of manganese poisoning on the proliferation of neural stem cells (NSCs) in mice's hippocampus.</p><p><b>METHODS</b>The mice (weight 8 approximately 10 g) were divided into control group(CG) low-dose group(LDG) middle-dose group(MDG) and high-dose group(HDG)by intraperitoneal injection of 0, 5, 20, 50 mg x kg(-1) x d(-1) of manganese chloride dissolved in physiological saline. The ability of learning and memory was detected by Morris Water Maze, and the proliferation of NSCs in subgranular zone (SGZ) in these mice's hippocampus was also detected by immunohistochemistry.</p><p><b>RESULTS</b>1) Compared with the CG, the ability of learning and memory in all manganism group decreased significantly (P < 0.01) and this phenomenon in HDG was most notable (P < 0.01). Meanwhile, the ability of memory was negatively correlated with the dose of manganese chloride (r(s) = -0.598, P < 0.01), but the difference of swimming speed in every group was of no statistic significance. (2) The numbers of NSCs in proliferation period in SGZ of all manganism groups was much lower than that of CG (P < 0.01) negatively correlated with the dose of manganese chloride (r(s) = -0.666, P < 0.01). (3) The reduction of NSCs had a positive correlation to the depression of learning and memory (r(s) = 0.734, P < 0.01).</p><p><b>CONCLUSIONS</b>Manganismus can affect the ability of learning and memory, which is probably caused by the inhalation of manganese on NSCs in hippocampus.</p>