- Email: [email protected]
Transient forebrain ischemia induces analgesia in the rat: Evidence for aα2-adrenoceptor mediated mechanism
S437
TRIGEMINAL NOCICEPTIVE NEUE@NS IN THE ITAMINAR NUCI@ OF ~y~~S.,&;;~~~of J;,if~;;p” N. W-a and Osaia Dental University, Osaka, Japan and Department of Physiology, Medical College of Shiga, Otsu, Japan.
BROWN Th-Fri ACC Hall E
. r. r AIM OF INVESTIGATION: In order to understand functional signirlcance or trigeminal nociceptive neurons in the intralaminar nuclei, their response characteristics were studied in the cat. Furthermore, it was attempted to identify neurons relaying trigeminal nociceptive input to the intralaminar nuclei and inhibition of synaptic transmission in nociceptive neurons of the intralaminar nuclei were examined following electrical stimulation of the nucleus raphe magnus (NRM) or of the periagueducal grey (PAG). METHODS: Experiments were carried out on cats anesthetized with urethane and chloralose. Single unit activities were recorded from the thalamus using glass capillary microelectrodes filled.with 2% pontamine sky blue in 1 M sodium acetate. RESULTS: Trigeminal nociceptive neurons were found in the nuclei centralis lateralis, paracentralis, centralis medialis, parafascicularis and subparafascicularis. They had a bilateral receptive field on the head. In addition, most of them were activated by noxious stimulation of the spinal nerve territory and by visceral sympathetic afferents. Following electrical stimulation of contralateral nucleus centralis lateralis , a majority of trigeminal nociceptive neurons in the dorsolateral part of the subnucleus reticularis ventralis of the caudal medulla oblongata were antidromically activated, suggesting that these nociceptive neurons relay trigeminal nociceptive input to the nucleus centralis lateralis. Responses of trigeminal nociceptive neurons in the intralaminar nuclei were inhibited following electrical stimulation of either the NRM or the PAG. CONCLUSION: Trigeminal nociceptive neurons were found in the intralaminar nuclei and their characteristics were clarified.
TRANSIENT FOREBRAIN ISCHEMIA INDUCES ANALGESIA IN THE RAT: BROWN Th-Fri Eyr;E;($ IF~RG;~~~~N;~~p MEVIED qC-SM..s. , M. Tiengo , K. Fuxe , L.F. Agnati 2 Y Inst. of Hur&n’Physiology, &iv. of Modena, vra Campi 287, Modena, Italy; Inst. of Physiopath+ogy & Therap of Pain, Univ. of Milan via Commenda 19,20122 Milan, Italy; Dept. of I&to rogy, Karolinska Inst., Stockholm 104 01, Sweden. Aim of Investigation; This study was undertaken to investigate the effects of transient forebrain ischemia on pain threshold in the rat. Methods: Transient forebrain ischemia (four-vessel occlusion, 4VO) was induced by permanent occlusion of vertebral arteries followed by temporary (30 min) occlusion of both carotid arteries. Forebrain ischemia was assessed by scoring EEG and gross behaviour in each animal carotid occlusion, and by histological evaluation of brain lesions at the end of the e hmdpaw licking was measured of naloxone, opiate antagonist, the@adrenoceptor antagonists selective 2-agonist (0.02-2 mg/ occlusion. Results; Transient forebrain ischemia induces strong hot plate analgesia in rats at 4h (latency in 4V0 rats=26.1+.8 set, sham operated rats= 10.6i.9 set), 1 and 2 days after the ischemic insult (pdl.01). Hot plate latency was significantly (@X05) higher in 4V0 rats when compared with sham operated rats up to 15 da s after forebrain ischemta. Yohimbine and idazoxan administration increased analgesia, whereas no ef rects was noted with naloxone and methysergide. Yohimbine effect in 4V0 was antagonized by clonidine pretreatment (0.7 mg/kg ip). In addition, low doses of clonidine (0.01-0.1 mk/kg ip) reduced the analgesia induced by forebrain tschemia in 4V0 rats to the values of sham operated ammals. Conclusion: A strong, time-dependent analgesia was observed in rats after transient forebrain ischemia. The pharmacological experiments suggest that an increase in central noradrenaline mediated transmission is specifically involved in the phenomenon of post-ischemic analgesia. In fact, low doses of clonidine are known to reduce central noradrenergic tone, while administration yohimbine or idazoxan increase central noradrenergic tone.
TRIGEMINAL NOCICEPTIVE NEUE@NS IN THE ITAMINAR NUCI@ OF ~y~~S.,&;;~~~of J;,if~;;p” N. W-a and Osaia Dental University, Osaka, Japan and Department of Physiology, Medical College of Shiga, Otsu, Japan.
BROWN Th-Fri ACC Hall E
. r. r AIM OF INVESTIGATION: In order to understand functional signirlcance or trigeminal nociceptive neurons in the intralaminar nuclei, their response characteristics were studied in the cat. Furthermore, it was attempted to identify neurons relaying trigeminal nociceptive input to the intralaminar nuclei and inhibition of synaptic transmission in nociceptive neurons of the intralaminar nuclei were examined following electrical stimulation of the nucleus raphe magnus (NRM) or of the periagueducal grey (PAG). METHODS: Experiments were carried out on cats anesthetized with urethane and chloralose. Single unit activities were recorded from the thalamus using glass capillary microelectrodes filled.with 2% pontamine sky blue in 1 M sodium acetate. RESULTS: Trigeminal nociceptive neurons were found in the nuclei centralis lateralis, paracentralis, centralis medialis, parafascicularis and subparafascicularis. They had a bilateral receptive field on the head. In addition, most of them were activated by noxious stimulation of the spinal nerve territory and by visceral sympathetic afferents. Following electrical stimulation of contralateral nucleus centralis lateralis , a majority of trigeminal nociceptive neurons in the dorsolateral part of the subnucleus reticularis ventralis of the caudal medulla oblongata were antidromically activated, suggesting that these nociceptive neurons relay trigeminal nociceptive input to the nucleus centralis lateralis. Responses of trigeminal nociceptive neurons in the intralaminar nuclei were inhibited following electrical stimulation of either the NRM or the PAG. CONCLUSION: Trigeminal nociceptive neurons were found in the intralaminar nuclei and their characteristics were clarified.
TRANSIENT FOREBRAIN ISCHEMIA INDUCES ANALGESIA IN THE RAT: BROWN Th-Fri Eyr;E;($ IF~RG;~~~~N;~~p MEVIED qC-SM..s. , M. Tiengo , K. Fuxe , L.F. Agnati 2 Y Inst. of Hur&n’Physiology, &iv. of Modena, vra Campi 287, Modena, Italy; Inst. of Physiopath+ogy & Therap of Pain, Univ. of Milan via Commenda 19,20122 Milan, Italy; Dept. of I&to rogy, Karolinska Inst., Stockholm 104 01, Sweden. Aim of Investigation; This study was undertaken to investigate the effects of transient forebrain ischemia on pain threshold in the rat. Methods: Transient forebrain ischemia (four-vessel occlusion, 4VO) was induced by permanent occlusion of vertebral arteries followed by temporary (30 min) occlusion of both carotid arteries. Forebrain ischemia was assessed by scoring EEG and gross behaviour in each animal carotid occlusion, and by histological evaluation of brain lesions at the end of the e hmdpaw licking was measured of naloxone, opiate antagonist, the@adrenoceptor antagonists selective 2-agonist (0.02-2 mg/ occlusion. Results; Transient forebrain ischemia induces strong hot plate analgesia in rats at 4h (latency in 4V0 rats=26.1+.8 set, sham operated rats= 10.6i.9 set), 1 and 2 days after the ischemic insult (pdl.01). Hot plate latency was significantly (@X05) higher in 4V0 rats when compared with sham operated rats up to 15 da s after forebrain ischemta. Yohimbine and idazoxan administration increased analgesia, whereas no ef rects was noted with naloxone and methysergide. Yohimbine effect in 4V0 was antagonized by clonidine pretreatment (0.7 mg/kg ip). In addition, low doses of clonidine (0.01-0.1 mk/kg ip) reduced the analgesia induced by forebrain tschemia in 4V0 rats to the values of sham operated ammals. Conclusion: A strong, time-dependent analgesia was observed in rats after transient forebrain ischemia. The pharmacological experiments suggest that an increase in central noradrenaline mediated transmission is specifically involved in the phenomenon of post-ischemic analgesia. In fact, low doses of clonidine are known to reduce central noradrenergic tone, while administration yohimbine or idazoxan increase central noradrenergic tone.