The Experts below are selected from a list of 1521 Experts worldwide ranked by ideXlab platform

Kiyokazu Ogita - One of the best experts on this subject based on the ideXlab platform.

  • beneficial effect of cilostazol mediated Neuronal Repair following trimethyltin induced Neuronal loss in the dentate gyrus
    Journal of Neuroscience Research, 2015
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Taro Yamaguchi, Masayuki Tanaka, Kiyokazu Ogita
    Abstract:

    Cilostazol acts as an antiplatelet agent and has other pleiotropic effects based on phosphodiesterase-3-dependent mechanisms. We evaluated whether cilostazol would have a beneficial effect on Neuronal Repair following hippocampal Neuronal damage by using a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus [Ogita et al. (2005) J Neurosci Res 82:609−621]; these mice will hereafter be referred to as impaired animals. A single treatment with cilostazol (10 mg/kg, i.p.) produced no significant change in the number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in the dentate granule cell layer (GCL) or subgranular zone on day 3 after TMT treatment. However, chronic treatment with cilostazol on days 3–15 posttreatment resulted in an increase in the number of BrdU-incorporating cells in the dentate GCL of the impaired animals, and these cells were positive for Neuronal nuclear antigen or doublecortin. Cilostazol was effective in elevating the level of phosphorylated cyclic adrenosine monophosphate response element-binding protein (pCREB) in the dentate gyrus of impaired animals. The results of a forced swimming test revealed that the chronic treatment with cilostazol improved the depression-like behavior seen in the impaired animals. In the cultures of hippocampal neural stem/progenitor cells, exposure to cilostazol produced not only enhancement of proliferation activity but also elevation of pCREB levels. Taken together, our data suggest that cilostazol has a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promotion of proliferation and/or Neuronal differentiation of neural progenitor cells in the subgranular zone. © 2014 Wiley Periodicals, Inc.

  • Beneficial effect of cilostazol‐mediated Neuronal Repair following trimethyltin‐induced Neuronal loss in the dentate gyrus
    Journal of Neuroscience Research, 2014
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Taro Yamaguchi, Masayuki Tanaka, Kiyokazu Ogita
    Abstract:

    Cilostazol acts as an antiplatelet agent and has other pleiotropic effects based on phosphodiesterase-3-dependent mechanisms. We evaluated whether cilostazol would have a beneficial effect on Neuronal Repair following hippocampal Neuronal damage by using a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus [Ogita et al. (2005) J Neurosci Res 82:609−621]; these mice will hereafter be referred to as impaired animals. A single treatment with cilostazol (10 mg/kg, i.p.) produced no significant change in the number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in the dentate granule cell layer (GCL) or subgranular zone on day 3 after TMT treatment. However, chronic treatment with cilostazol on days 3–15 posttreatment resulted in an increase in the number of BrdU-incorporating cells in the dentate GCL of the impaired animals, and these cells were positive for Neuronal nuclear antigen or doublecortin. Cilostazol was effective in elevating the level of phosphorylated cyclic adrenosine monophosphate response element-binding protein (pCREB) in the dentate gyrus of impaired animals. The results of a forced swimming test revealed that the chronic treatment with cilostazol improved the depression-like behavior seen in the impaired animals. In the cultures of hippocampal neural stem/progenitor cells, exposure to cilostazol produced not only enhancement of proliferation activity but also elevation of pCREB levels. Taken together, our data suggest that cilostazol has a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promotion of proliferation and/or Neuronal differentiation of neural progenitor cells in the subgranular zone. © 2014 Wiley Periodicals, Inc.

  • lithium promotes Neuronal Repair and ameliorates depression like behavior following trimethyltin induced Neuronal loss in the dentate gyrus
    PLOS ONE, 2014
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Kasumi Umeda, Taro Yamaguchi, Kiyokazu Ogita
    Abstract:

    Lithium, a mood stabilizer, is known to ameliorate the stress-induced decrease in hippocampal neurogenesis seen in animal models of stress-related disorders. However, it is unclear whether lithium has beneficial effect on Neuronal Repair following Neuronal damage in Neuronal degenerative diseases. Here, we evaluated the effect of in vivo treatment with lithium on the hippocampal Neuronal Repair in a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus (such mice referred to as “impaired animals”) [Ogita et al. (2005) J Neurosci Res 82: 609–621]. The impaired animals had a dramatically increased number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in their dentate gyrus at the initial time window (days 3 to 5 post-TMT treatment) of the self-Repair stage. A single treatment with lithium produced no significant change in the number of BrdU-incorporating cells in the dentate granule cell layer and subgranular zone on day 3 post-TMT treatment. On day 5 post-TMT treatment, however, BrdU-incorporating cells were significantly increased in number by lithium treatment for 3 days. Most interestingly, chronic treatment (15 days) with lithium increased the number of BrdU-incorporating cells positive for NeuN or doublecortin in the dentate granule cell layer of the impaired animals, but not in that of naive animals. The results of a forced swimming test revealed that the chronic treatment with lithium improved the depression-like behavior seen in the impaired animals. Taken together, our data suggest that lithium had a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promoted proliferation and survival/Neuronal differentiation of neural stem/progenitor cells in the subgranular zone.

Seeram Ramakrishna - One of the best experts on this subject based on the ideXlab platform.

  • application of conductive polymers scaffolds and electrical stimulation for nerve tissue engineering
    Journal of Tissue Engineering and Regenerative Medicine, 2011
    Co-Authors: Laleh Ghasemimobarakeh, Mohammad Hossein Nasresfahani, Hossein Baharvand, Sahar Kiani, Salem S Aldeyab, Mohammad Morshed, Molamma P. Prabhakaran, Seeram Ramakrishna
    Abstract:

    Among the numerous attempts to integrate tissue engineering concepts into strategies to Repair nearly all parts of the body, Neuronal Repair stands out. This is partially due to the complexity of the nervous anatomical system, its functioning and the inefficiency of conventional Repair approaches, which are based on single components of either biomaterials or cells alone. Electrical stimulation has been shown to enhance the nerve regeneration process and this consequently makes the use of electrically conductive polymers very attractive for the construction of scaffolds for nerve tissue engineering. In this review, by taking into consideration the electrical properties of nerve cells and the effect of electrical stimulation on nerve cells, we discuss the most commonly utilized conductive polymers, polypyrrole (PPy) and polyaniline (PANI), along with their design and modifications, thus making them suitable scaffolds for nerve tissue engineering. Other electrospun, composite, conductive scaffolds, such as PANI/gelatin and PPy/poly(e-caprolactone), with or without electrical stimulation, are also discussed. Different procedures of electrical stimulation which have been used in tissue engineering, with examples on their specific applications in tissue engineering, are also discussed. Copyright © 2011 John Wiley & Sons, Ltd.

Florence M Bareyre - One of the best experts on this subject based on the ideXlab platform.

  • Neuronal Repair and replacement in spinal cord injury
    Journal of the Neurological Sciences, 2008
    Co-Authors: Florence M Bareyre
    Abstract:

    Abstract Spinal cord injury (SCI) often induces loss of motor and/or sensory function below the level of injury. While deficits persist in complete lesions, partial lesions of the spinal cord can be followed by spontaneous functional recovery. In this review we address the mechanisms underlying spontaneous recovery in the adult CNS. We argue that the adult brain and spinal cord are able to spontaneously respond to SCI, and do so by (i) anatomically reorganizing axonal connections and (ii) generating new precursor cells. Knowledge of the endogenous recovery strategies should also provide the basis for the development of new therapeutic strategies for spinal cord injury. In this review we describe the processes of endogenous axonal Repair and cell replacement in the injured spinal cord and discuss how transplantation of stem/progenitor cells could enhance these endogenous Repair strategies.

Masanori Yoneyama - One of the best experts on this subject based on the ideXlab platform.

  • beneficial effect of cilostazol mediated Neuronal Repair following trimethyltin induced Neuronal loss in the dentate gyrus
    Journal of Neuroscience Research, 2015
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Taro Yamaguchi, Masayuki Tanaka, Kiyokazu Ogita
    Abstract:

    Cilostazol acts as an antiplatelet agent and has other pleiotropic effects based on phosphodiesterase-3-dependent mechanisms. We evaluated whether cilostazol would have a beneficial effect on Neuronal Repair following hippocampal Neuronal damage by using a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus [Ogita et al. (2005) J Neurosci Res 82:609−621]; these mice will hereafter be referred to as impaired animals. A single treatment with cilostazol (10 mg/kg, i.p.) produced no significant change in the number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in the dentate granule cell layer (GCL) or subgranular zone on day 3 after TMT treatment. However, chronic treatment with cilostazol on days 3–15 posttreatment resulted in an increase in the number of BrdU-incorporating cells in the dentate GCL of the impaired animals, and these cells were positive for Neuronal nuclear antigen or doublecortin. Cilostazol was effective in elevating the level of phosphorylated cyclic adrenosine monophosphate response element-binding protein (pCREB) in the dentate gyrus of impaired animals. The results of a forced swimming test revealed that the chronic treatment with cilostazol improved the depression-like behavior seen in the impaired animals. In the cultures of hippocampal neural stem/progenitor cells, exposure to cilostazol produced not only enhancement of proliferation activity but also elevation of pCREB levels. Taken together, our data suggest that cilostazol has a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promotion of proliferation and/or Neuronal differentiation of neural progenitor cells in the subgranular zone. © 2014 Wiley Periodicals, Inc.

  • Beneficial effect of cilostazol‐mediated Neuronal Repair following trimethyltin‐induced Neuronal loss in the dentate gyrus
    Journal of Neuroscience Research, 2014
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Taro Yamaguchi, Masayuki Tanaka, Kiyokazu Ogita
    Abstract:

    Cilostazol acts as an antiplatelet agent and has other pleiotropic effects based on phosphodiesterase-3-dependent mechanisms. We evaluated whether cilostazol would have a beneficial effect on Neuronal Repair following hippocampal Neuronal damage by using a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus [Ogita et al. (2005) J Neurosci Res 82:609−621]; these mice will hereafter be referred to as impaired animals. A single treatment with cilostazol (10 mg/kg, i.p.) produced no significant change in the number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in the dentate granule cell layer (GCL) or subgranular zone on day 3 after TMT treatment. However, chronic treatment with cilostazol on days 3–15 posttreatment resulted in an increase in the number of BrdU-incorporating cells in the dentate GCL of the impaired animals, and these cells were positive for Neuronal nuclear antigen or doublecortin. Cilostazol was effective in elevating the level of phosphorylated cyclic adrenosine monophosphate response element-binding protein (pCREB) in the dentate gyrus of impaired animals. The results of a forced swimming test revealed that the chronic treatment with cilostazol improved the depression-like behavior seen in the impaired animals. In the cultures of hippocampal neural stem/progenitor cells, exposure to cilostazol produced not only enhancement of proliferation activity but also elevation of pCREB levels. Taken together, our data suggest that cilostazol has a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promotion of proliferation and/or Neuronal differentiation of neural progenitor cells in the subgranular zone. © 2014 Wiley Periodicals, Inc.

  • lithium promotes Neuronal Repair and ameliorates depression like behavior following trimethyltin induced Neuronal loss in the dentate gyrus
    PLOS ONE, 2014
    Co-Authors: Masanori Yoneyama, Tatsuo Shiba, Shigeru Hasebe, Kasumi Umeda, Taro Yamaguchi, Kiyokazu Ogita
    Abstract:

    Lithium, a mood stabilizer, is known to ameliorate the stress-induced decrease in hippocampal neurogenesis seen in animal models of stress-related disorders. However, it is unclear whether lithium has beneficial effect on Neuronal Repair following Neuronal damage in Neuronal degenerative diseases. Here, we evaluated the effect of in vivo treatment with lithium on the hippocampal Neuronal Repair in a mouse model of trimethyltin (TMT)-induced Neuronal loss/self-Repair in the hippocampal dentate gyrus (such mice referred to as “impaired animals”) [Ogita et al. (2005) J Neurosci Res 82: 609–621]. The impaired animals had a dramatically increased number of 5-bromo-2′-deoxyuridine (BrdU)-incorporating cells in their dentate gyrus at the initial time window (days 3 to 5 post-TMT treatment) of the self-Repair stage. A single treatment with lithium produced no significant change in the number of BrdU-incorporating cells in the dentate granule cell layer and subgranular zone on day 3 post-TMT treatment. On day 5 post-TMT treatment, however, BrdU-incorporating cells were significantly increased in number by lithium treatment for 3 days. Most interestingly, chronic treatment (15 days) with lithium increased the number of BrdU-incorporating cells positive for NeuN or doublecortin in the dentate granule cell layer of the impaired animals, but not in that of naive animals. The results of a forced swimming test revealed that the chronic treatment with lithium improved the depression-like behavior seen in the impaired animals. Taken together, our data suggest that lithium had a beneficial effect on Neuronal Repair following Neuronal loss in the dentate gyrus through promoted proliferation and survival/Neuronal differentiation of neural stem/progenitor cells in the subgranular zone.

Hannah C Kinney - One of the best experts on this subject based on the ideXlab platform.

  • potential Neuronal Repair in cerebral white matter injury in the human neonate
    Pediatric Research, 2011
    Co-Authors: Robin L Haynes, Gang Xu, Rebecca D Folkerth, Felicia L Trachtenberg, Joseph J Volpe, Hannah C Kinney
    Abstract:

    Periventricular leukomalacia (PVL) in the premature infant represents the major substrate underlying cognitive deficits and cerebral palsy and is characterized as focal periventricular necrosis and diffuse gliosis in the immature cerebral white matter. We have recently shown a significant decrease in the density of neurons in PVL relative to controls throughout the white matter, including the subventricular, periventricular, and subcortical regions. These neurons are likely to be remnants of the subplate and/or GABAergic neurons in late migration to the cerebral cortex, both of which are important for proper cortical circuitry in development and throughout adulthood. Here, we tested the hypothesis that intrinsic Repair occurs in PVL to attempt to compensate for the deficits in white matter neurons. By using doublecortin (DCX) immunopositivity as a marker of postmitotic migrating neurons, we found significantly increased densities (p < 0.05) of DCX-immunopositive cells in PVL cases (n = 9) compared with controls (n = 7) in the subventricular zone (their presumed site of origin), necrotic foci, and subcortical white matter in the perinatal time-window, i.e. 35–42 postconceptional weeks. These data provide the first evidence suggestive of an attempt at Neuronal Repair or regeneration in human neonatal white matter injury.