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1004 Central injection of prostaglandin E2 induces thermalhyper algesia in rats; possible involvement of EP3 receptors
SIO0 1002 ELECTROPHYSIOLOGICAL STUDIES ON THE AUTONOMIC INNERVATION OF THE T H Y M U S A N D L Y M P H N O D E I N T H E RAT. A K I R A N I I J I M A , D e p a r t m e n t of P h y s i o l . , N i i g a t a U n i v e r s i t y S c h o o l of M e d . , N i i g a t a 951 Japan. It has been pointed out that the autonomic outflows play important roles in modulation of immune function. In this context electrophysiological studies were conducted to investigate vagal innervation of the thymus and splanchnic (sympathetic) innervation of the mesenteric lymph node. Efferent discharges were recorded from the nerve filament dissected from the central cut end of the vagal branch innervating the thymus or splanchnic branch innervating the mesenteric lympn node in urethaneahesthetized rat. An i.v. injection of IL-I~ (10ng, 0.1ml) resulted in a facilitation of the efferent outflows in both of these nerves which usually lasted longe r than 90 min. Stimulation of the cervical vagus evoked action potentials in the thymus branch of the vagus nerve, and that of splanchnic nerve provoked action potentials in the mesenteric nerve innervating the lymph node, indicating C-fiber group with their conduction velocities (~im/sec).
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IN SITU HYBRIDIZATION STUDY OF TYPE 1 INTERLEUKIN-1 RECEPTOR mRNA IN THE RAT BRAIN. KAZUKI Y A B U U C H I l ,MASABUMI MINAMII AND MASAMICHI SATOH2, 1Department of Pharmacology and 2Department of Molecular Pharmacology, Facul .ty of Pharmaceutical Sciences, Kyoto Universi .ty, Kyoto 606-01, Japan
Intedeukin-1 (IL-1) is a cytokine which has been reported to act within the central nervous system to modify neuronal and glial functions. In this study, to examine the regions where type 1 IL-1 receptor (IL-1R1) mRNA was expressed in the rat brain, in situ hybridization study was conducted. IL-1R1 mRNA was expressed in the olfactory bulb, cerebral cortex, amygdala, thalamus, hypothalamus and cerebellar Purkinje cells. In these areas, IL-1R1 mRNA was expressed mainly on the cells which have large nucleus and lightly stained with cresyl violet, probably neurons. Furthermore, it was intensely expressed on the vascular endothelial cells and epithelial cells of ventricles. In addition, we have previously reported that IL-113 mRNA was markedly induced by the treatment with kainie acid in above mentioned regions. These results suggest that central IL-1 might primarily act on neurons to modulate neuronal activities. Furthermore, the fact that IL-1R1 m R N A is expressed on the endothelial ceils suggest that peripheral IL-1 might affect the central functions via endothelial cells.
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CENTRAL INJECTION OF PROSTAGLANDIN E2 INDUCES THERMAL HYPERALGESIA IN RATS; POSSIBLE INVOLVEMENT OF EP3 RECEPTORS. TAKAKAZU OKA, SHUJI AOU AND TETSURO HORI, Department of Physiology, Kyushu University Faculty of Medicine, Fukuoka, 812 Japan. Previous reports on the central effect of prostaglandin E2 (PGE2) on nociception is controversial, by which both analgesia and hyperalgesia are suggested. To determine the central effect of PGE2 on nociception and which type of prostanoid receptors is involved in the PGE2-induced.changes.in nociception, we administered PGE2 and its agonists, i.e., 17-phenyl trinor PGE2 (an EPI receptor agonist), butaprost (an EP2 agonist) and M&B28767 (an EP3 agonist) into the lateral cerebroventricle (i.c.v.) in rats and observed the changes in paw -withdrawal latency on a hot plate. Non-pyrogenic doses of PGE2 (10pg/kg- 1ng/kg) and M&B28767 (10pg/kg-100pg/kg) induced significant reduction in paw-withdrawal latency. The maximal reductions were obtained 15 min after i.c.v, injection of both drugs. 17-phenyl trinor PGE2 (lpg/kg-1/~ g/kg) or butaprost (lpg/kg-1 p g/kg) induced fro significant changes in paw-withdrawal latency. A pyrogenic dose of PGE2 (I/.(g/kg) increased the latency 5 min after injection. However, a pyrogenic dose of 17-phenyl trinor PGE2 (1/~ g/kg) did not change it. The results indicate that non-pyrogenic doses of PGrb enhance thermal nociception.through EP3 receptors by its central action in rats.
1003
IN SITU HYBRIDIZATION STUDY OF TYPE 1 INTERLEUKIN-1 RECEPTOR mRNA IN THE RAT BRAIN. KAZUKI Y A B U U C H I l ,MASABUMI MINAMII AND MASAMICHI SATOH2, 1Department of Pharmacology and 2Department of Molecular Pharmacology, Facul .ty of Pharmaceutical Sciences, Kyoto Universi .ty, Kyoto 606-01, Japan
Intedeukin-1 (IL-1) is a cytokine which has been reported to act within the central nervous system to modify neuronal and glial functions. In this study, to examine the regions where type 1 IL-1 receptor (IL-1R1) mRNA was expressed in the rat brain, in situ hybridization study was conducted. IL-1R1 mRNA was expressed in the olfactory bulb, cerebral cortex, amygdala, thalamus, hypothalamus and cerebellar Purkinje cells. In these areas, IL-1R1 mRNA was expressed mainly on the cells which have large nucleus and lightly stained with cresyl violet, probably neurons. Furthermore, it was intensely expressed on the vascular endothelial cells and epithelial cells of ventricles. In addition, we have previously reported that IL-113 mRNA was markedly induced by the treatment with kainie acid in above mentioned regions. These results suggest that central IL-1 might primarily act on neurons to modulate neuronal activities. Furthermore, the fact that IL-1R1 m R N A is expressed on the endothelial ceils suggest that peripheral IL-1 might affect the central functions via endothelial cells.
"[0 0 4
CENTRAL INJECTION OF PROSTAGLANDIN E2 INDUCES THERMAL HYPERALGESIA IN RATS; POSSIBLE INVOLVEMENT OF EP3 RECEPTORS. TAKAKAZU OKA, SHUJI AOU AND TETSURO HORI, Department of Physiology, Kyushu University Faculty of Medicine, Fukuoka, 812 Japan. Previous reports on the central effect of prostaglandin E2 (PGE2) on nociception is controversial, by which both analgesia and hyperalgesia are suggested. To determine the central effect of PGE2 on nociception and which type of prostanoid receptors is involved in the PGE2-induced.changes.in nociception, we administered PGE2 and its agonists, i.e., 17-phenyl trinor PGE2 (an EPI receptor agonist), butaprost (an EP2 agonist) and M&B28767 (an EP3 agonist) into the lateral cerebroventricle (i.c.v.) in rats and observed the changes in paw -withdrawal latency on a hot plate. Non-pyrogenic doses of PGE2 (10pg/kg- 1ng/kg) and M&B28767 (10pg/kg-100pg/kg) induced significant reduction in paw-withdrawal latency. The maximal reductions were obtained 15 min after i.c.v, injection of both drugs. 17-phenyl trinor PGE2 (lpg/kg-1/~ g/kg) or butaprost (lpg/kg-1 p g/kg) induced fro significant changes in paw-withdrawal latency. A pyrogenic dose of PGE2 (I/.(g/kg) increased the latency 5 min after injection. However, a pyrogenic dose of 17-phenyl trinor PGE2 (1/~ g/kg) did not change it. The results indicate that non-pyrogenic doses of PGrb enhance thermal nociception.through EP3 receptors by its central action in rats.