Role of thalamic ventral posterolateral nucleus histamine H 2 and opiate receptors in modulation of formalin-induced muscle pain in rats

摘要

Highlights ? Intramuscular injection of formalin produced paw licking and paw flinching. ? Ranitidine prevented histamine-, dimaprit- and morphine-antinociception. ? Naloxone blocked morphine-, histamine-, and dimaprit-induced antinociception. ? Histamine H 2 and opiate receptors modulate muscle pain at the PVL level. Abstract Background Histamine and opiate systems contribute to supraspinal processing of pain. In the present study, we investigated the effects of microinjection of histamine and agonists and antagonists of histamine H 2 and opiate receptors into the thalamic ventral posterolateral nucleus on muscle pain in rats. Methods The thalamic ventral posterolateral nuclei were bilaterally implanted with two guide cannulas. Muscle pain was induced by intramuscular injection of a diluted formalin solution (2.5%, 50μl) into the belly of gastrocnemius muscle, and pain-related behaviors including paw licking duration and paw flinching number were recorded at five-min blocks for 60min. Results Formalin produced a biphasic pattern of pain-related behaviors. Ranitidine (a histamine H 2 receptor antagonist) alone did not affect pain intensity, whereas it prevented the antinociceptive activities of histamine, dimaprit (a histamine H 2 receptor agonist) and morphine (an opiate receptor agonist). Naloxone (an opiate receptor antagonist) alone increased pain, and inhibited histamine-, dimaprit-, and morphine-induced antinociception. Locomotor activity was not changed with these chemicals. Conclusions Our results showed an interaction between histamine H 2 and opiate receptors at the thalamic ventral posterolateral nucleus in modulation of muscle pain.