Neuroscience
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Neurogenesis in the substantia nigra (SN) has been a controversial issue. Here we report that neurogenesis can be induced in the adult rodent SN by transplantation of embryoid body cells (EBCs) derived from mouse embryonic stem cells. The detection of Sox2+ dividing (BrdU+) putative host neural precursor cells (NPCs) between 1 and 6 days post-transplantation (dpt) supported the neurogenic capacity of the adult SN. ⋯ Remarkably, new blood vessels formed in association with the neurogenic process that, when precluded, caused a reduction in neuroblast production. Accordingly, two proteins secreted by EBCs, Fgf2 and Vegf, were able to promote the emergence of Dcx+/Psa-Ncam+, Tubb3+ and NeuN+/BrdU+ cells in vivo in the absence of EBCs. We propose that the adult SN is a mostly silent neurogenic niche with the ability to generate new neurons by typical and atypical mechanisms.
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Understanding the neural mechanisms of training-induced brain plasticity has significant implications for improving academic achievement. Previous studies suggest abacus-based mental calculation (AMC) training significantly improves individual's arithmetic capability, and the frontal-parietal network is suggested to be the key neural circuit underlying AMC. Yet, it remains unclear how AMC training shifts brain activation in this network and whether the training effect is transferable or not. ⋯ The control group, on the other hand, did not exhibit any pre- to post-training differences in brain activation on any of the three tasks. These findings extend the previous cross-sectional studies of AMC and suggest that AMC training induces functional changes in brain activation and such plasticity may be transferable beyond the AMC. The training effects on sustained and transient neural activity may also provide a new perspective to understand training-induced neural plasticity and related transfer effect.
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μ-Opioid Receptor Activation Directly Modulates Intrinsically Photosensitive Retinal Ganglion Cells.
Intrinsically photosensitive retinal ganglion cells (ipRGCs) encode light intensity and trigger reflexive responses to changes in environmental illumination. In addition to functioning as photoreceptors, ipRGCs are post-synaptic neurons in the inner retina, and there is increasing evidence that their output can be influenced by retinal neuromodulators. Here we show that opioids can modulate light-evoked ipRGC signaling, and we demonstrate that the M1, M2 and M3 types of ipRGCs are immunoreactive for μ-opioid receptors (MORs) in both mouse and rat. ⋯ Recordings from solitary ipRGCs, enzymatically dissociated from retinas obtained from melanopsin-driven fluorescent reporter mice, confirmed that DAMGO exerts its effect directly through MORs expressed by ipRGCs. Reduced ipRGC excitability occurred via modulation of voltage-gated potassium and calcium currents. These findings suggest a potential new role for endogenous opioids in the mammalian retina and identify a novel site of action-MORs on ipRGCs-through which opioids might exert effects on reflexive responses to environmental light.
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Holistic face processing is a critical component of face recognition. There are two classical measures of holistic face processing: the whole-part effect (WPE) and composite-face effect (CFE). However, the two effects have demonstrated inconsistent pattern of results in behavioral literature. ⋯ These results suggested that the WPE was related to integration of the rOFA within the CFN, while the CFE was associated with separation of the rFFA from other CFN regions. Further analyses showed that higher WPE was related to stronger connection between the rOFA and bilateral posterior superior temporal sulcus (pSTS), while larger CFE was associated with weaker connection between the rFFA and bilateral pSTS. In short, our study reveals distinct neural correlates of the two hallmarks of holistic face processing at network level and sheds new light on the different mechanisms of holistic face processing reflected by the two effects.
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Oxysterol derived from cholesterol metabolism is involved in the inflammatory activation, and consequently in development of major chronic diseases. Multiple cytokines have been found to induce the expression of cholesterol metabolism-related enzymes. Several studies have shown that the protein level of cholesterol-25-hydroxylase (CH25H) is remarkably increased in response to injury of central nervous system (CNS), but little is known about the mechanisms of cytokine-induced expression of CH25H in specific cell types, and the resultant effects. ⋯ MIF facilitated ch25h expression of astrocytes through interaction with CD74 membrane receptor, which in turn promoted production of chemokines, as identified by transcriptome profiles. MIF-induced release of oxysterol 25-hydroxycholesterol (25-HC) from astrocytes affects cell migration, but inhibited cell viability in dose-dependent manner, suggesting that MIF aggravates progressive neuropathology through regulation of cholesterol metabolism following CNS injury. These results have provided a novel mechanism and a potential therapeutic strategy for injured CNS.