Abstract
Objective: The present study was performed to explore the role of mu opioid receptor (MOR) in nociceptive modulation in anterior cingulate cortex (ACC) of rats with inflammatory pain. Methods: To set up an inflammatory pain model, rats received a subcutaneous injection of 0.1 ml of 2% carrageenan into the left hindpaw. The hindpaw withdrawal latency (HWL) to thermal and mechanical stimulation, by hot plate and Randall Selitto Test respectively, was used to evaluate the rat's responses to noxious stimulation. The effects induced by intra-ACC administration of morphine and opioid receptor antagonists were observed. The influence of inflammatory pain on MOR mRNA level and MOR expression in ACC were assayed by Reverse Transcription Polymerase Chain Reaction (RT-PCR) and western blot. Results: We found that intra-ACC administration of morphine induced significant antinociceptive effects in a dose-dependent manner in rats with inflammatory pain. Furthermore, the antinociceptive effects induced by morphine were attenuated by intra-ACC injection of the opioid receptor antagonist naloxone, indicating an involvement of opioid receptor in nociceptive modulation in ACC in rats with inflammatory pain. Moreover, intra-ACC administration of the MOR antagonist β-funaltrexamine (β-FNA) attenuated the morphine-induced antinociception significantly in rats with inflammatory pain. The results demonstrated that blockade MOR by β-FNA inhibited the morphine-induced antinociception, indicating that MOR plays an important role in nociceptive modulation in ACC in rats with inflammatory pain. We further found that the morphine-induced antinociception was lower in rats with inflammatory pain than that in normal rats. Interestingly, we found that there were significant decreases in MOR mRNA level and MOR expression in ACC in rats with inflammatory pain compared with intact rats tested by RT-PCR and western blot, indicating that there is a down regulation in MOR expression in rats with inflammatory pain, which support our above results that morphine-induced antinociception was lower in rats with inflammatory pain than that in normal rats. Conclusion: These findings suggest that MOR plays an important role in nociceptive modulation in ACC in rats with inflammatory pain and there is a down-regulation in MOR expression in rats with inflammatory pain.
Highlights
Lots of studies have demonstrated that anterior cingulate cortex (ACC) is involved in acute and chronic pain [1,2,3,4,5,6]
These results demonstrated that blockade mu opioid receptor (MOR) by β-FNA inhibited the morphine-induced antinociception significantly, indicating that MOR plays an important role in nociceptive modulation in ACC in rats with inflammatory pain
We found that the morphine-induced antinociception was lower in rats with inflammatory pain than that in normal rats, which suggests that opioid receptors might be changed by making inflammatory pain model
Summary
Lots of studies have demonstrated that anterior cingulate cortex (ACC) is involved in acute and chronic pain [1,2,3,4,5,6] Ikeda and her colleagues found that the activation of astrocytes in the ACC plays a crucial role in the development of negative emotions and LTP during pain hypersensitivity after peripheral inflammation [4]. Zhao and her colleagues found that calmodulin-stimulated adenylyl cyclases (AC), AC-1 and/or AC-8, were crucial in mediating the long-lasting enhanced presynaptic transmitter release in the ACC of mice with chronic pain [5].
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