| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Research Abstract |
Our experiments by the end of last fiscal year revealed that in an isolated rat hemisected spinal cord model, nociceptin suppresses the wind-up phenomenon induced by repeated application of an electric stimulus and that the suppresson is not antagonized by a classic, opioid antagonist naloxone. In order to further clarify the physiological roles of the nociceptin receptor, any relationships between the nociceptin and other anti-nociception-related receptors including the cholinergic system and any effect of nociceptin on the respiratory center located in the medulla oblongata were investigated this fiscal year. That is as follows. After an isolated rat medulla oblongata-spinal cord model was prepared and irrigated with artificial cerebrospinal fluid (aCSF) (27.5 C, pH 7.4), nociceptin (0 nM, 10 nM, 30 nM, 100 nM and 1 microM, dissolved in the aCSF) was applied to the preparation. It dose-dependently suppressed the respiration-related potential which was recorded from the ventral root of the fourth cervical nerve. This suppression was not reversed by naloxone. Accordingly, it is indicated that the nociceptin receptor play physiological roles in a variety of the central nervous system, not through classical opioid receptor subtypes. On the other hand, in an isolated rat spinal cord model, carbachol suppressed pain-related slow ventral root potential from the lumbar spinal cord induced by an electric stimulus to the dorsal root. This suppression was reversed by co-administration with atropine, and the muscarinic receptor was found to play an important role for this suppression. Similar suppression by carbachol for motor-related monosynaptic reflex potential (MSR) was not reversed by idazoxane or naloxone, and MSR suppressed by carbachol is not likely to have relationships with such kinds of receptors.
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