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We have recently demonstrated that N(6)-cyclopentyladenosine (CPA), an adenosine A1 receptor agonist, acts centrally to induce a visceral antinociception. Since serotonin (5-HT), cannabinoid (CB), dopamine or opioid signaling in the central nervous system is involved in the regulation of visceral sensation, we made a hypothesis that the signaling may play a role in the CPA-induced visceral antinociception. Visceral sensation was evaluated by colonic distension-induced abdominal withdrawal reflex (AWR) in conscious rats. Subcutaneously administered CPA significantly increased the threshold of colonic distension-induced AWR. Intracisternal injection of either 5-HT or 5-HT receptor antagonist blocked the CPA-induced visceral antinociception while 5-HT antagonist did not block the CPA-induced visceral antinociception. Subcutaneous injection of dopamine D receptor antagonist, CB receptor antagonist or naloxone significantly blocked the CPA-induced visceral antinociception while neither subcutaneous injection of dopamine D receptor antagonist nor CB receptor antagonist blocked the CPA-induced anti-pain action. These results suggest that 5-HT, 5-HT, dopamine D, CB receptors and the opioid system in the CNS may specifically mediate the CPA-induced visceral antinociception. These findings may help in understanding the physiological relevance of central adenosine with special reference to the pathophysiology of altered visceral sensation especially in irritable bowel syndrome.
This article was published in the following journal.
Name: Physiology & behavior
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