Vanilloid VR1 receptor is involved in rimonabant-induced neuroprotection.

摘要: Recently, a potential neuroprotective effect of rimonabant, independent the CB1 receptor interaction, has been proposed. In present study, role transient channel vanilloid subfamily member 1, named VR1, on global cerebral ischemia in gerbils, was investigated. Rimonabant (0.05-3 mg kg-1), given i.p. 5 min after recirculation, dose dependently antagonized ischemia-induced decrease electroencephalographic (EEG) total spectral power and restored relative frequency band distribution 7 days ischemia. (0.125-0.5 kg-1) fully prevented hyperlocomotion 1 day memory impairment evaluated passive avoidance task, 3 At ischemia, survival pyramidal cells, CA1 subfield, respectively 91 96%, animals rimonabant 0.25 0.5 kg-1, compared to vehicle group. Higher doses were not protective. The protection induced by followed bell-shaped curve, maximal active being kg-1. Capsazepine (0.01 selective VR1 antagonist, completely reversed rimonabant-induced effects against EEG flattening, hippocampal neuronal loss. These findings suggest that receptors are involved rimonabant's neuroprotection even if other mechanisms can contribute this effect.