In normal animals, spinal administration of
neuropeptide Y induces
analgesia to thermal stimuli, but has no effect on mechanical thresholds. Recent anatomical studies, however, have shown that following nerve injury there is an altered expression of
neuropeptide Y and its receptors. The aim of this behavioural study, therefore, is to examine the effect of intrathecal administration of
neuropeptide Y, its agonists and an antagonist on mechanical nociceptive thresholds in rats with partial injury to the sciatic nerve. Test agents were administered for 14 days via osmotic pumps (0.5 microliter/day) attached to intrathecal
catheters and the nociceptive flexion reflex was quantified using an Ugo Basile Analgesymeter. Partial injury to the sciatic nerve, in animals treated intrathecally with saline, induces a significant decrease in mechanical threshold as compared to the
sham operated, contralateral paw. The nerve injury-induced
hyperalgesia is exacerbated by 2 microM
neuropeptide Y and by 2 microM [Leu31,Pro34]-
neuropeptide Y, a Y1 receptor agonist. The Y2 receptor agonist, N-acetyl-[Leu28,Leu31]-
neuropeptide Y24-36 (2 microM), had no effect on the nerve injury-induced
hyperalgesia. The putative
neuropeptide Y antagonist,
alpha-trinositol (10 microM), significantly attenuated the nerve injury-induced
hyperalgesia. This study suggests that
neuropeptide Y may contribute to nerve injury-induced
mechanical hyperalgesia via the Y1 receptor and provides further insight into the possible mechanisms underlying nerve injury-induced
hyperalgesia to mechanical stimuli.