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저널/프로시딩 상세정보

권호별목차 / 소장처보기

H : 소장처정보

T : 목차정보

Neuroscience 45건

  1. [해외논문]   Novel genes in brain tissues of EAE-induced normal and obese mice: Upregulation of metal ion-binding protein genes in obese-EAE mice  

    Hasan, M. ; Seo, J.E. ; Rahaman, K.A. ; Min, H. ; Kim, K.H. ; Park, J.H. ; Sung, C. ; Son, J. ; Kang, M.J. ; Jung, B.H. ; Park, W.S. ; Kwon, O.S.
    Neuroscience v.343 ,pp. 322 - 336 , 2017 , 0306-4522 ,

    초록

    Experimental autoimmune encephalomyelitis (EAE) is an inflammatory autoimmune disease of the central nervous system resulting from degeneration of the myelin sheath. This study is aimed to identify differentially expressed genes (DEGs) in the brain of EAE-induced normal diet (ND) mice and high-fat diet (HFD)-induced obese mice, and to identify novel genes responsible for elucidating the mechanism of the disease. Purified mRNA samples from the brain tissue were analyzed for gene microarray and validated by real-time RT-PCR. DEGs were identified if significant changes greater than 1.5-fold or less than 0.66-fold were observed (p

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  2. [해외논문]   TFP5 is comparable to mild hypothermia in improving neurological outcomes in early-stage ischemic stroke of adult rats  

    Ji, Y.B. ; Zhuang, P.P. ; Ji, Z. ; Huang, K.B. ; Gu, Y. ; Wu, Y.M. ; Pan, S.Y. ; Hu, Y.F.
    Neuroscience v.343 ,pp. 337 - 345 , 2017 , 0306-4522 ,

    초록

    Aim: We compared the efficacy of a modified truncated 24-aa peptide (TFP5), derived from the cyclin-dependent kinase 5 (CDK5)-activating cofactor p35, with mild hypothermia (MH), and determined whether the efficacy of TFP5 is affected by MH. Methods: Ischemic stroke was induced in adult male Sprague-Dawley rats for 2h. Immediately after initiating reperfusion, TFP5, MH, or the combination of the two were administrated. 48h after reperfusion, neurological outcomes were evaluated. Results: Rats that received either MH, TFP5, or the combined treatment showed smaller brain infarct size than normothermia control (NT), and there was no apparent difference among these three treatment groups. The neurological deficit was significantly improved only by the combined treatment. MH or TFP5 ameliorated the blood-brain barrier (BBB) disruption in ischemic regions with similar efficacy, whereas the combination of them had a trend toward better effect. Besides, the cleavage of p35 into p25 and apoptosis in ischemic regions was inhibited by TFP5 or the combination, but not by MH alone. Conclusions: TFP5 is comparable to MH in improving neurological outcomes in early-stage adult ischemic stroke. When TFP5 is given along with MH, less neurological deficit tends to be achieved.

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  3. [해외논문]   Amygdalar and hippocampal connections with brainstem and spinal cord: A diffusion MRI study in human brain  

    Arrigo, A. ; Mormina, E. ; Calamuneri, A. ; Gaeta, M. ; Marino, S. ; Milardi, D. ; Anastasi, G.P. ; Quartarone, A.
    Neuroscience v.343 ,pp. 346 - 354 , 2017 , 0306-4522 ,

    초록

    The limbic system has a central role for the integration of several cognitive and visceral functions through an extended network of connections involving the hippocampus and the amygdala. A number of studies performed in humans have been dedicated to the investigation of supratentorial limbic pathways by means of non-invasive MRI approaches, such as DTI. However, detection of possible limbic connections involving the brainstem and the spinal cord is still missing. Subtentorial limbic pathways have been previously studied in animals by means of invasive approaches, including viral tracing. The detection of limbic connections with the brainstem and the spinal cord has raised several new hypotheses regarding the interaction between the central nervous system and the periphery of the body. We investigated subtentorial limbic connections in twenty-one healthy humans by means of probabilistic constrained spherical deconvolution tractography. Our connectivity analysis showed, for both the hippocampus and the amygdala, a high probability of connections with the midbrain, pons, and bulb. Moreover, hippocampal and amygdalar pathways reaching the cervical spinal cord were also detected. Quantitative evaluation of diffusion parameters was also performed. Findings of the present study are in agreement with the literature and provide the first report of possible limbic connections between the brainstem and the spinal cord in human brain. Since these pathways might also have important implications both in physiological and pathological contexts, further studies should be conducted in order to confirm our data as well as to define functional features of these brain connections.

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  4. [해외논문]   Immunolocalization of glutaryl-CoA dehydrogenase (GCDH) in adult and embryonic rat brain and peripheral tissues  

    Braissant, O. ; Jafari, P. ; Remacle, N. ; Cudre-Cung, H.P. ; Do Vale Pereira, S. ; Ballhausen, D.
    Neuroscience v.343 ,pp. 355 - 363 , 2017 , 0306-4522 ,

    초록

    Glutaryl-CoA dehydrogenase (GCDH) is a mitochondrial enzyme that is involved in the degradation of tryptophan, lysine and hydroxylysine. Deficient enzyme activity leads to glutaric aciduria type-I (GA-I). This neurometabolic disease usually manifests with acute encephalopathic crises and striatal neuronal death in early childhood leading to an irreversible dystonic-dyskinetic movement disorder. Fronto-temporal atrophy and white matter changes are already present in the pre-symptomatic period. No detailed information on GCDH expression during embryonic development and in adulthood was available so far. Using immunofluorescence microscopy and cell-type-specific markers to localize GCDH in different tissues, we describe the differential cellular localization of GCDH in adult rat brain and peripheral organs as well as its spatiotemporal expression pattern. During embryonic development GCDH was predominantly expressed in neurons of the central and peripheral nervous system. Significant expression levels were found in epithelial cells (skin, intestinal and nasal mucosa) of rat embryos at different developmental stages. Besides the expected strong expression in liver, GCDH was found to be significantly expressed in neurons of different brain regions, renal proximal tubules, intestinal mucosa and peripheral nerves of adult rats. GCDH was found widely expressed in embryonic and adult rat tissues. In rat embryos GCDH is predominantly expressed in brain implying an important role for brain development. Interestingly, GCDH was found to be significantly expressed in different other organs (e.g. kidney, gut) in adult rats probably explaining the evolving phenotype in GA-I patients.

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  5. [해외논문]   Apolipoprotein E4 causes early olfactory network abnormalities and short-term olfactory memory impairments  

    Peng, K.Y. ; Mathews, P.M. ; Levy, E. ; Wilson, D.A.
    Neuroscience v.343 ,pp. 364 - 371 , 2017 , 0306-4522 ,

    초록

    While apolipoprotein (Apo) E4 is linked to increased incidence of Alzheimer's disease (AD), there is growing evidence that it plays a role in functional brain irregularities that are independent of AD pathology. However, ApoE4-driven functional differences within olfactory processing regions have yet to be examined. Utilizing knock-in mice humanized to ApoE4 versus the more common ApoE3, we examined a simple olfactory perceptual memory that relies on the transfer of information from the olfactory bulb (OB) to the piriform cortex (PCX), the primary cortical region involved in higher order olfaction. In addition, we have recorded in vivo resting and odor-evoked local field potentials (LPF) from both brain regions and measured corresponding odor response magnitudes in anesthetized young (6-month-old) and middle-aged (12-month-old) ApoE mice. Young ApoE4 compared to ApoE3 mice exhibited a behavioral olfactory deficit coinciding with hyperactive odor-evoked response magnitudes within the OB that were not observed in older ApoE4 mice. Meanwhile, middle-aged ApoE4 compared to ApoE3 mice exhibited heightened response magnitudes in the PCX without a corresponding olfactory deficit, suggesting a shift with aging in ApoE4-driven effects from OB to PCX. Interestingly, the increased ApoE4-specific response in the PCX at middle-age was primarily due to a dampening of baseline spontaneous activity rather than an increase in evoked response power. Our findings indicate that early ApoE4-driven olfactory memory impairments and OB network abnormalities may be a precursor to later network dysfunction in the PCX, a region that not only is targeted early in AD, but may be selectively vulnerable to ApoE4 genotype.

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  6. [해외논문]   Wnt signaling promotes axonal regeneration following optic nerve injury in the mouse  

    Patel, A.K. ; Park, K.K. ; Hackam, A.S.
    Neuroscience v.343 ,pp. 372 - 383 , 2017 , 0306-4522 ,

    초록

    Adult mammalian CNS axons generally do not regenerate, creating an obstacle to effective repair and recovery after neuronal injury. The canonical Wnt/β-catenin signaling pathway is an essential signal transduction cascade that regulates axon growth and neurite extension in the developing mammalian embryo. In this study, we investigated whether a Wnt/β-catenin signaling activator could be repurposed to induce regeneration in the adult CNS after axonal injury. We used a retinal ganglion cell (RGC) axon crush injury model in a transgenic Wnt reporter mouse, and intravitreal injections were used to deliver Wnt3a or saline to the RGC cell bodies within the retina. Our findings demonstrated that Wnt3a induced Wnt signaling in RGCs and resulted in significant axonal regrowth past the lesion site when measured at two and four weeks post-injury. Furthermore, Wnt3a-injected eyes showed increased survival of RGCs and significantly higher pattern electroretinography (PERG) amplitudes compared to the control. Additionally, Wnt3a-induced axonal regeneration and RGC survival were associated with elevated activation of the transcription factor Stat3, and reducing expression of Stat3 using a conditional Stat3 knock-out mouse line led to diminished Wnt3a-dependent axonal regeneration and RGC survival. Therefore, these findings reveal a novel role for retinal Wnt signaling in axonal regrowth and RGC survival following axonal injury, which may lead to the development of novel therapies for axonal regeneration.

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  7. [해외논문]   Stress induces equivalent remodeling of hippocampal spine synapses in a simulated postpartum environment and in a female rat model of major depression  

    Baka, J. ; Csakvari, E. ; Huzian, O. ; Dobos, N. ; Siklos, L. ; Leranth, C. ; MacLusky, N.J. ; Duman, R.S. ; Hajszan, T.
    Neuroscience v.343 ,pp. 384 - 397 , 2017 , 0306-4522 ,

    초록

    Stress and withdrawal of female reproductive hormones are known risk factors of postpartum depression. Although both of these factors are capable of powerfully modulating neuronal plasticity, there is no direct electron microscopic evidence of hippocampal spine synapse remodeling in postpartum depression. To address this issue, hormonal conditions of pregnancy and postpartum period were simulated in ovariectomized adult female Sprague-Dawley rats (n=76). The number of hippocampal spine synapses and the depressive behavior of rats in an active escape task were investigated in untreated control, hormone-withdrawn 'postpartum', simulated proestrus, and hormone-treated 'postpartum' animals. After 'postpartum' withdrawal of gonadal steroids, inescapable stress caused a loss of hippocampal spine synapses, which was related to poor escape performance in hormone-withdrawn 'postpartum' females. These responses were equivalent with the changes observed in untreated controls that is an established animal model of major depression. Maintaining proestrus levels of ovarian hormones during 'postpartum' stress exposure did not affect synaptic and behavioral responses to inescapable stress in simulated proestrus animals. By contrast, maintaining pregnancy levels of estradiol and progesterone during 'postpartum' stress exposure completely prevented the stress-induced loss of hippocampal spine synapses, which was associated with improved escape performance in hormone-treated 'postpartum' females. This protective effect appears to be mediated by a muted stress response as measured by serum corticosterone concentrations. In line with our emerging 'synaptogenic hypothesis' of depression, the loss of hippocampal spine synapses may be a novel perspective both in the pathomechanism and in the clinical management of postpartum affective illness.

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  8. [해외논문]   ASIC channel inhibition enhances excitotoxic neuronal death in an in vitro model of spinal cord injury  

    Mazzone, G.L. ; Veeraraghavan, P. ; Gonzalez-Inchauspe, C. ; Nistri, A. ; Uchitel, O.D.
    Neuroscience v.343 ,pp. 398 - 410 , 2017 , 0306-4522 ,

    초록

    In the spinal cord high extracellular glutamate evokes excitotoxic damage with neuronal loss and severe locomotor impairment. During the cell dysfunction process, extracellular pH becomes acid and may activate acid-sensing ion channels (ASICs) which could be important contributors to neurodegenerative pathologies. Our previous studies have shown that transient application of the glutamate analog kainate (KA) evokes delayed excitotoxic death of spinal neurons, while white matter is mainly spared. The present goal was to enquire if ASIC channels modulated KA damage in relation to locomotor network function and cell death. Mouse spinal cord slices were treated with KA (0.01 or 0.1mM) for 1h, and then washed out for 24h prior to analysis. RT-PCR results showed that KA (at 0.01mM concentration that is near-threshold for damage) increased mRNA expression of ASIC1a, ASIC1b, ASIC2 and ASIC3, an effect reversed by the ASIC inhibitor 4',6-diamidino-2-phenylindole (DAPI). A KA neurotoxic dose (0.1mM) reduced ASIC1a and ASIC2 expression. Cell viability assays demonstrated KA-induced large damage in spinal slices from mice with ASIC1a gene ablation. Likewise, immunohistochemistry indicated significant neuronal loss when KA was followed by the ASIC inhibitors DAPI or amiloride. Electrophysiological recording from ventral roots of isolated spinal cords showed that alternating oscillatory cycles were slowed down by 0.01mMKA, and intensely inhibited by subsequently applied DAPI or amiloride. Our data suggest that early rise in ASIC expression and function counteracted deleterious effects on spinal networks by raising the excitotoxicity threshold, a result with potential implications for improving neuroprotection.

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  9. [해외논문]   Assessing human brain impedance using simultaneous surface and intracerebral recordings  

    Ranta, R. ; Le Cam, S. ; Tyvaert, L. ; Louis-Dorr, V.
    Neuroscience v.343 ,pp. 411 - 422 , 2017 , 0306-4522 ,

    초록

    Most of the literature on the brain impedance proposes a frequency-independent resistive model. Recently, this conclusion was tackled by a series of papers (Bedard et al., 2006; Bedard and Destexhe, 2009; Gomes et al., 2016), based on microscopic sale modeling and measurements. Our paper aims to investigate the impedance issue using simultaneous in vivo depth and surface signals recorded during intracerebral electrical stimulation of epileptic patients, involving a priori different tissues with different impedances. Our results confirm the conclusions from Logothethis et al. (2007): there is no evidence of frequency dependence of the brain tissue impedance (more precisely, there is no difference, in terms of frequency filtering, between the brain and the skull bone), at least at a macroscopic scale. In order to conciliate findings from both microscopic and macroscopic scales, we recall different neural/synaptic current generators' models from the literature and we propose an original computational model, based on fractional dynamics.

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  10. [해외논문]   Polyunsaturated fatty acid biostatus, phospholipase A2 activity and brain white matter microstructure across adolescence  

    McNamara, R.K. ; Szeszko, P.R. ; Smesny, S. ; Ikuta, T. ; DeRosse, P. ; Vaz, F.M. ; Milleit, B. ; Hipler, U.C. ; Wiegand, C. ; Hesse, J. ; Amminger, G.P. ; Malhotra, A.K. ; Peters, B.D.
    Neuroscience v.343 ,pp. 423 - 433 , 2017 , 0306-4522 ,

    초록

    Adolescence is a period of major brain white matter (WM) changes, and membrane lipid metabolism likely plays a critical role in brain WM myelination. Long-chain polyunsaturated fatty acids (LC-PUFAs) are essential components of cell membranes including oligodendrocytes, and LC-PUFA release and turnover in membranes is regulated by phospholipase A 2 enzymes. To investigate the role of membrane lipid metabolism in healthy WM myelination across adolescence, the present study examined the relationship between membrane LC-PUFA biostatus, phospholipase A 2 activity, and brain WM microstructure in healthy subjects aged 9-20years (n=30). Diffusion tensor imaging (DTI) was performed to measure average fractional anisotropy (FA) and diffusivity (indices sensitive to WM myelination) of nine major cerebral WM tracts. Blood samples were collected to measure erythrocyte membrane fatty acid concentrations and plasma intracellular phospholipase A 2 activity (inPLA 2 ). Plasma inPLA 2 activity showed a significant U-curved association with WM radial diffusivity, and an inverted U-curved association with WM FA, independent of age. A significant positive linear correlation was observed between docosahexaenoic acid concentration and axial diffusivity in the corpus callosum. These findings suggest that there may be optimal physiological inPLA 2 activity levels associated with healthy WM myelination in late childhood and adolescence. Myelination may be mediated by cleavage of docosahexaenoic acid from membrane phospholipids by inPLA 2 . These findings have implications for our understanding of the role of LC-PUFA homeostasis in myelin-related neurodevelopmental disorders.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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