Abstract |
Nociceptin and its N-terminal fragment, nociceptin (1 7), were administered intrathecally (i.t.) into conscious mice. Nociceptin (3.0 fmol) produced a significant reduction in the nociceptive thermal threshold ( hyperalgesia) measured as the tail-flick and paw-withdrawal responses. Nociceptin (1-7), injected i.t., at 150-1200 fmol had no significant effect. However, when nociceptin (1-7) (150 1200 fmol) was injected simultaneously with nociceptin (3.0 fmol), nociceptin-induced hyperalgesia was significantly reduced. Analgesia induced by a high dose (1200 pmol) of nociceptin was not antagonized by co-administration of nociceptin (1-7) (1200 fmol). These results suggest that N-terminal fragments of nociceptin formed endogenously could modulate the hyperalgesic action of nociceptin in the spinal cord.
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Authors | T Sakurada, S Sakurada, S Katsuyama, C Sakurada, K Tan-No, L Terenius |
Journal | British journal of pharmacology
(Br J Pharmacol)
Vol. 128
Issue 5
Pg. 941-4
(Nov 1999)
ISSN: 0007-1188 [Print] England |
PMID | 10556929
(Publication Type: Journal Article)
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Chemical References |
- Opioid Peptides
- Peptide Fragments
- Receptors, Opioid
- nociceptin
- Nociceptin Receptor
- Oprl1 protein, mouse
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Topics |
- Amino Acid Sequence
- Animals
- Hyperalgesia
(chemically induced, prevention & control)
- Injections, Intraventricular
- Injections, Spinal
- Male
- Mice
- Molecular Sequence Data
- Opioid Peptides
(antagonists & inhibitors)
- Pain Measurement
(drug effects)
- Peptide Fragments
(administration & dosage, chemical synthesis, pharmacology)
- Reaction Time
(drug effects)
- Receptors, Opioid
(metabolism)
- Spinal Cord
(drug effects, metabolism)
- Nociceptin Receptor
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