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Neuroprotection induced by vitamin E against oxidative stress in hippocampal neurons: involvement of TRPV1 channels.

Abstract : Pretreatment of cultured hippocampal neurons with a low concentration of alpha-tocopherol (alpha-TP), the major component of vitamin E, results in a long-lasting protection against oxidative damages, via genomic effects. This neuroprotection is associated with the attenuation of a calcium influx triggered by oxidative agents such as Fe(2+) ions. This Ca(2+) influx is supported by a TRP-like channel, also partly involved in capacitive calcium entry within neurons. Here, we evidence the contribution of TRPV1 channels in this mechanism. TRPV1 channels are activated by various agents including capsaicin, the pungent component of hot chili peppers and blocked by capsazepine (CPZ) or 5'-iodo-resiniferatoxin. Both TRPV1 inhibitors strongly reduced Fe(2+) ion-mediated toxicity and Ca(2+) influx, in the same way as to alpha-TP pretreatment. Moreover, CPZ also decreased capacitive calcium entry in hippocampal neurons. Finally, both CPZ and 5'-iodo-resiniferatoxin reduced spontaneous excitatory synaptic transmission; this depression of synaptic transmission being largely occluded in alpha-TP-pretreated neurons. In conclusion, in our experimental model, TRPV1 channels are involved in the Fe(2+) ion-induced neuronal death and a negative modulation of this channel activity by alpha-TP pretreatment may account, at least in part, for the long-lasting neuroprotection against oxidative stress.
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Contributor : Janique Guiramand Connect in order to contact the contributor
Submitted on : Tuesday, April 20, 2010 - 4:55:00 PM
Last modification on : Tuesday, December 21, 2021 - 11:00:02 AM

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Nadine Crouzin, Marie-Céleste de Jesus Ferreira, Catherine Cohen-Solal, Gérard Barbanel, Janique Guiramand, et al.. Neuroprotection induced by vitamin E against oxidative stress in hippocampal neurons: involvement of TRPV1 channels.. Molecular Nutrition and Food Research, Wiley-VCH Verlag, 2010, 54 (4), pp.496-505. ⟨10.1002/mnfr.200900188⟩. ⟨hal-00474703⟩



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