Neurocentre Magendie

Yu ZHANG





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13 publication(s) depuis Juin 2000:


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Les IF indiqués ont été collectés par le Web of Sciences en


10/11/2014 | Nat Neurosci   IF 16.7
Dendritic channelopathies contribute to neocortical and sensory hyperexcitability in Fmr1 mice.
Zhang Y*, Bonnan A*, Bony G*, Ferezou I, Pietropaolo S, Ginger M, Sans N, Rossier J, Oostra B, Lemasson G, Frick A

Abstract:
Hypersensitivity in response to sensory stimuli and neocortical hyperexcitability are prominent features of Fragile X Syndrome (FXS) and autism spectrum disorders, but little is known about the dendritic mechanisms underlying these phenomena. We found that the primary somatosensory neocortex (S1) was hyperexcited in response to tactile sensory stimulation in Fmr1-/y mice. This correlated with neuronal and dendritic hyperexcitability of S1 pyramidal neurons, which affect all major aspects of neuronal computation, from the integration of synaptic input to the generation of action potential output. Using dendritic electrophysiological recordings, calcium imaging, pharmacology, biochemistry and a computer model, we found that this defect was, at least in part, attributable to the reduction and dysfunction of dendritic h- and BKCa channels. We pharmacologically rescued several core hyperexcitability phenomena by targeting BKCa channels. Our results provide strong evidence pointing to the utility of BKCa channel openers for the treatment of the sensory hypersensitivity aspects of FXS.




11/2008 | Brain Behav Immun   IF 5.9
Minocycline suppresses morphine-induced respiratory depression, suppresses morphine-induced reward, and enhances systemic morphine-induced analgesia.
Hutchinson MR, Northcutt AL, Chao LW, Kearney JJ, Zhang Y, Berkelhammer DL, Loram LC, Rozeske RR, Bland ST, Maier SF, Gleeson TT, Watkins LR

Abstract:
Recent data suggest that opioids can activate immune-like cells of the central nervous system (glia). This opioid-induced glial activation is associated with decreased analgesia, owing to the release of proinflammatory mediators. Here, we examine in rats whether the putative microglial inhibitor, minocycline, may affect morphine-induced respiratory depression and/or morphine-induced reward (conditioned place preference). Systemic co-administration of minocycline significantly attenuated morphine-induced reductions in tidal volume, minute volume, inspiratory force, and expiratory force, but did not affect morphine-induced reductions in respiratory rate. Minocycline attenuation of respiratory depression was also paralleled with significant attenuation by minocycline of morphine-induced reductions in blood oxygen saturation. Minocycline also attenuated morphine conditioned place preference. Minocycline did not simply reduce all actions of morphine, as morphine analgesia was significantly potentiated by minocycline co-administration. Lastly, morphine dose-dependently increased cyclooxygenase-1 gene expression in a rat microglial cell line, an effect that was dose-dependently blocked by minocycline. Together, these data support that morphine can directly activate microglia in a minocycline-suppressible manner and suggest a pivotal role for minocycline-sensitive processes in the mechanisms of morphine-induced respiration depression, reward, and pain modulation.




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2008 | Nanoscale Res. Lett.   IF 2.9
Subcellular Localization of Thiol-Capped CdTe Quantum Dots in Living Cells
Zhang Y, Mi L, Xiong R, Wang P, Chen J, Yang W, Wang C, Peng Q

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2008 | Small   IF 8.3
Photoluminescence decay dynamics of thiol-capped CdTe quantum dots in living cells under microexcitation
Zhang Y, Mi L, Wang P, Lu S, Chen J, Guo J, Yang W, Wang C

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2007 | Anal Chim Acta   IF 4.7
Tracking of mercury ions in living cells with a fluorescent chemodosimeter under single- or two-photon excitation
Lu Z, Wang P, Zhang Y, Chen J, Zhen S, Leng B, Tian H

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2007 | J Phys Chem B   IF 3.2
Photochemical instability of thiol-capped CdTe quantum dots in aqueous solution and living cells: Process and mechanism
Ma J, Chen J, Zhang Y, Wang P, Guo J, Yang W, Wang C

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