In:
Molecular Nutrition & Food Research, Wiley, Vol. 54, No. 4 ( 2010-04), p. 496-505
Abstract:
Pretreatment of cultured hippocampal neurons with a low concentration of alpha‐tocopherol (α‐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 α‐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 α‐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 α‐TP pretreatment may account, at least in part, for the long‐lasting neuroprotection against oxidative stress.
Type of Medium:
Online Resource
ISSN:
1613-4125
,
1613-4133
DOI:
10.1002/mnfr.200900188
Language:
English
Publisher:
Wiley
Publication Date:
2010
detail.hit.zdb_id:
2160372-8
SSG:
12
