Elsevier

Neuroscience Letters

Volume 292, Issue 2, 6 October 2000, Pages 83-86
Neuroscience Letters

Nociceptin attenuates opioid and γ-aminobutyric acidB receptor-mediated analgesia in the mouse tail-flick assay

https://doi.org/10.1016/S0304-3940(00)01448-8Get rights and content

Abstract

Nociceptin (NC) and the opioid receptor like-1 receptors are widely distributed in areas of the neuraxis that are part of the descending modulatory pain system. We used the tail-flick assay in mice to assess the interaction between NC and other analgesic compounds acting on different areas of the descending pathway. Given by intracerebroventricular injection, NC induced hyperalgesia at 10 nmol (39% of reduction vs. control group). The same dose of NC reversed analgesia induced by distinct classes of analgesia-producing compounds such as morphine, dynorphin A or baclofen. NC caused a reduction of their antinociceptive effects: 61, 41 and 27%, respectively. Thus, NC at the supraspinal level appears to interact with both opioid and γ-aminobutyric acidB systems producing anti-analgesic effects probably through the descending pathway for pain control.

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Acknowledgements

We would like to thank Dr Ennio Ongini for his critical comments on the manuscript.

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    or in specific brain regions known to mediate the analgesic actions of μ-opioid drugs. OFQ/N also attenuates opioid and non-opioid stress-induced analgesia and acupuncture analgesia, and interferes with the analgesic effects of the alpha2-adrenergic agonist clonidine and the GABAB agonist baclofen (Mogil et al., 1996a,b; King et al., 1998; Suaudeau et al., 1998; Wang et al., 1999b; Citterio et al., 2000; Grisel and Mogil, 2000; Rizzi et al., 2001b). In contrast, as discussed in depth in a recent review (Mogil and Pasternak, 2001), the reported effects of OFQ/N per se on nociceptive responses are quite varied.

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Present address: ENDO Pharmaceuticals Inc., 1333 Campus Parkway Neptune, NJ, USA.

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