tail flick modification of orexin-a induced changes of electrophysiological parameters in the rostral ventromedial medulla

objective: it is well known that intracerebroventricular (icv) and supraspinal injections of orexin-a elicit analgesia, but the mechanism(s) of action remains unidentified. this study aims to characterize the effect of orexin-a on rostral ventromedial medulla (rvm) neurons which are involved in the descending nociception modulating pathway. materials and methods: in this experimental study, we injected orexin-a or vehicle directly into rats’ icv while the tail flick (tf) latencies were measured and the on- and off-cell firing activities were monitored for more than 60 minutes. results: in response to noxious stimuli on the tail, we observed increased firing rate of on-cells and a decreased association with the firing rate of off-cells and in neutral cells the firing rate was unchanged just prior to tail flicking. icv injection of orexin-a decreased the spontaneous firing rate of on-cells (the type of rvm neurons believed to have facilitatory action on nociception). furthermore, orexin-a increased firing rate of off-cells (the type of rvm neurons believed to have an inhibitory action on nociception). orexin-a reduced the tf-related responses of on-cells and tf-related pause duration of off-cells. conclusion: these results have shown that the analgesic effect produced by orexin-a may be induced by brainstem neurons. it is suggested that the orexinergic system from the hypothalamus to the rvm may have a potential role in modulation of nociceptive transmission.