The Experts below are selected from a list of 84 Experts worldwide ranked by ideXlab platform

Gilbert Grima - One of the best experts on this subject based on the ideXlab platform.

  • glutamate induced release of the nitric oxide precursor arginine from glial cells
    European Journal of Neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q Do
    Abstract:

    : Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.

  • Glutamate‐induced Release of the Nitric Oxide Precursor, Arginine, From Glial Cells
    The European journal of neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q.
    Abstract:

    Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.

Kim Q. - One of the best experts on this subject based on the ideXlab platform.

  • Glutamate‐induced Release of the Nitric Oxide Precursor, Arginine, From Glial Cells
    The European journal of neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q.
    Abstract:

    Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.

Kim Q Do - One of the best experts on this subject based on the ideXlab platform.

  • glutamate induced release of the nitric oxide precursor arginine from glial cells
    European Journal of Neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q Do
    Abstract:

    : Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.

Jon Robbins - One of the best experts on this subject based on the ideXlab platform.

  • The calcium influx pathway in rat olfactory ensheathing cells shows TRPC channel pharmacology
    Brain research, 2004
    Co-Authors: Richard Davies, Shaista Hayat, Caroline B. Wigley, Jon Robbins
    Abstract:

    Pharmacological characterisation of the calcium influx pathway in olfactory ensheathing cells (OECs) was performed using Indo-1 calcium microfluorometry. Our previous work has implicated this pathway in olfactory ensheathing cell support for regeneration of axons from adult CNS neurons. In high extracellular calcium (20 mM), cumulative concentration inhibition curves were generated for Lu(3+), Gd(3+) and econazole, giving IC(50)s of 0.09, 1.51 and 1.13 microM, respectively, and slope values that were not significantly different from unity. Combining these results with those obtained previously, an order of inhibitor potency was found to be Lu(3+)>La(3+)=econazole=Gd(3+)>1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride (SKF96365)>Cd(2+). This profile most closely fits some members of the TRPC family of non-voltage gated calcium influx channels and may indicate that a TRP-mediated calcium influx plays a role in Glial-Neuronal Interaction and axonal regeneration.

  • Short communication The calcium influx pathway in rat olfactory ensheathing cells shows TRPC channel pharmacology
    2004
    Co-Authors: Richard Davies, Shaista Hayat, Caroline B. Wigley, Jon Robbins
    Abstract:

    AbstractPharmacological characterisation of the calcium influx pathway in olfactory ensheathing cells (OECs) was performed using Indo-1calcium microfluorometry. Our previous work has implicated this pathway in olfactory ensheathing cell support for regeneration of axonsfrom adult CNS neurons. In high extracellular calcium (20 mM), cumulative concentration inhibition curves were generated for Lu 3+ ,Gdand econazole, giving IC 50 s of 0.09, 1.51 and 1.13 AM, respectively, and slope values that were not significantly different from unity.Combining these results with those obtained previously, an order of inhibitor potency was found to be Lu 3+ NLa 3+ =econazole=Gd 3+ N1-[2-(4-methoxyphenyl)-2-[3-(4-methoxyphenyl)propoxy]ethyl-1H-imidazole hydrochloride (SKF96365)NCd 2+ . This profile most closely fits somemembers of the TRPC family of non-voltage gated calcium influx channels and may indicate that a TRP-mediated calcium influx plays a rolein glial–neuronal Interaction and axonal regeneration.D 2004 Elsevier B.V. All rights reserved.

B Benz - One of the best experts on this subject based on the ideXlab platform.

  • glutamate induced release of the nitric oxide precursor arginine from glial cells
    European Journal of Neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q Do
    Abstract:

    : Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.

  • Glutamate‐induced Release of the Nitric Oxide Precursor, Arginine, From Glial Cells
    The European journal of neuroscience, 1997
    Co-Authors: Gilbert Grima, B Benz, Kim Q.
    Abstract:

    Arginine, the nitric oxide precursor, is predominantly localized in glial cells, whereas the constitutive nitric oxide synthase is mainly found in neurons. Therefore, a transfer of arginine from glial cells to neurons is needed to replenish the neuronal precursor pool. This is further supported by the finding that arginine is released upon selective pathway stimulation both in vitro and in vivo. We investigated the mechanism underlying this Glial-Neuronal Interaction by analysing the effect of glutamate receptor agonists on the extracellular [3H]arginine level in cerebellar and cortical slices and in cultures of either cortical astroglial cells or neurons. We present data indicating that arginine is released from cerebellar and cortical slices and astroglial cell cultures upon activation of ionotropic non-NMDA glutamate receptors. Glutamate had no effect on the extracellular [3H]arginine level in neuronal cultures. Moreover, the effect of glutamate in cerebellar slices was tetrodotoxin-insensitive, and the calcium ionophore A23187 evoked the release of [3H]arginine from astroglial cell cultures. Thus, nitric oxide synthesis and nitric oxide transmission may be based on the Glial-Neuronal transfer of arginine which is induced by activation of excitatory amino acid receptors on glial cells.