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Regeneration of pyramidal tract following transection in the rat
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REGENERATION OF PYRAMlDAL TRACT FOLLOWING TRANSECTION IN THE RAT. TATSUSHI INOUE1*2, SABURO KAWAGUCHI’, ‘Dept. of Integrative Bmin Science, Faculty of Medicine, Kyoto Univ., Kyoto 606, Japan,ZDept. of Neurosurgery, Faculty of Medicine, Hiroshima Univ., Hiroshima 723, Japan. Regeneration of the pyramidal tract after transection has been reported in the infant hamster (Kalil and Reh,Science 205)in which the regenerated axons did not pass through the lesion but formed dispersed aberrant pathways coursing around the lesion. We tested this in the rat. Under pentobarbital(4Omg/kg, i.p.) or cooling anesthesia, the medullary pyramid of infant
rats (8 to 28 post natal days) were completely transected unilaterally by ventral approach through an opening in the basioccipital bone. After the post-operative interval of 4 days to 9 months, the pyramidal tract was examined by the anterograde tracing method with WGA-HRP that was injected unilaterally in the sensorimotor cortex ipsilateralto the lesion. Even in the animals of 20 to 28 days of age, much older than in the previous report on hamster (4 to 8 days of age), marked regeneration occurred through the lesion. The regenerated fibers formd a compact fiber bundle, formed the pyramidal decussation, traversed through the contralateral dorsal column giving terminals to normal targets, and reached the sacral segments as normal. The results indicate the occurrence of genuine regeneration of severed axons but not of redirected growth of developing fibers as argued against the aberrant pyramidal tract in the hamster (Tolbert and Der, J. Comp. Neurol. 260).
1303
DEXAMETHASONE ENHANCES EXPRESSION OF GAP-43 mRNA AFTER NERVE INJURY AND FACILITATES RE-INNERVATION OF THE HYPOGLOSSAL NERVE. GUI-LAN YAO AND HIROSHI KIYAMA, Dent.of Neuroanatomv.Biomedical Research Center, Qsaka Univ.Sch.of Med. Yamadaoka. Suita.Osaka 565.JAPAN.
Application of dexamethasone was found to induce an enhanced expression of mRNA encoding the growth associated protein (GAP-43)after peripheral nerve injury. Following hypoglossal nerve axotomy, a dexamethasone releasing pellet (1.5 mg released in 3 weeks) was placed near the transected nerve. GAP-43 mRNA was detected in the hypoglossal nucleus by non-radioactive in situ hybridization histochemistry using an alkaline phosphatase-labeled oligonucleotide probe.A significant elevation of GAP43mFLNA level was observed 2 weeks after the transection in dexamethasone treated animals. This induction was not observed in the dorsal motor nucleus of vagus which expresses moderately high levels of GAP-43 mFUJA even without nerve injury. Although dexamethasone did not alter the maximum level of GAP-43 mRNA in the hypoglossal nucleus after nerve injury, it prolonged the period in which the mRNA expression remained elevated. This may be due to post-transcriptional effect by the glucocorticoid. Dexamethasone treatment also caused a slight facilitation of reinnervation. This seems due to the enhancement of GAP-43 mRNA level by the glucocorticoid.
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c-Fos induction in the superficial dorsal horn by formalin stimulation of the adult rat hindpaw following tibia1 nerve crush Akihiro Yoshidal)z), Hiroyuki Ichikawaz), Tomosada Sugimotoz), Oral and Maxillofacial Surgery II), Oral Anatomy 112), Okayama Uni\ J.Sch. of Dent. Sikata-cho, Okayama, 700, Japan Formalin injection into the hindpaw of rats induces rapid c-Fos expression throughout the 2 days earlier selectively terminal field of the sciatic primary neurons. The tibia1 neurotomy eliminates the c-Fos induction in the medial part of sciatic terminal field (tibia1 territory) and, thereby, enables one to assess the responsiveness of dorsal horn neurons to noxicious primary input through the spared peroneal nerve. When the tibia1 nerve had been crushed 12days before the tibia1 neurotomy, many neurons in the tibia1 territory yielded stimulus-induced c-Fos expression. Therefore, the deafferented dorsal horn neurons in the tibia1 territory responded by c-Fos expression to somatotopically in appropriate (peroneal) primary input. When the nerve had been crushed 19 days before the neurotomy, such ectopic c-Fos inducibility had subsided. The regenerated tibia1 primary neurons were capable of transganglionic transport of WGA-HRP from the hindpaw at 19 days but not 12 days after the nerve crush. Normal dorsal horn somatotopy map is desrupted by a peripheral nerve injury and restored by regeneration.
REGENERATION OF PYRAMlDAL TRACT FOLLOWING TRANSECTION IN THE RAT. TATSUSHI INOUE1*2, SABURO KAWAGUCHI’, ‘Dept. of Integrative Bmin Science, Faculty of Medicine, Kyoto Univ., Kyoto 606, Japan,ZDept. of Neurosurgery, Faculty of Medicine, Hiroshima Univ., Hiroshima 723, Japan. Regeneration of the pyramidal tract after transection has been reported in the infant hamster (Kalil and Reh,Science 205)in which the regenerated axons did not pass through the lesion but formed dispersed aberrant pathways coursing around the lesion. We tested this in the rat. Under pentobarbital(4Omg/kg, i.p.) or cooling anesthesia, the medullary pyramid of infant
rats (8 to 28 post natal days) were completely transected unilaterally by ventral approach through an opening in the basioccipital bone. After the post-operative interval of 4 days to 9 months, the pyramidal tract was examined by the anterograde tracing method with WGA-HRP that was injected unilaterally in the sensorimotor cortex ipsilateralto the lesion. Even in the animals of 20 to 28 days of age, much older than in the previous report on hamster (4 to 8 days of age), marked regeneration occurred through the lesion. The regenerated fibers formd a compact fiber bundle, formed the pyramidal decussation, traversed through the contralateral dorsal column giving terminals to normal targets, and reached the sacral segments as normal. The results indicate the occurrence of genuine regeneration of severed axons but not of redirected growth of developing fibers as argued against the aberrant pyramidal tract in the hamster (Tolbert and Der, J. Comp. Neurol. 260).
1303
DEXAMETHASONE ENHANCES EXPRESSION OF GAP-43 mRNA AFTER NERVE INJURY AND FACILITATES RE-INNERVATION OF THE HYPOGLOSSAL NERVE. GUI-LAN YAO AND HIROSHI KIYAMA, Dent.of Neuroanatomv.Biomedical Research Center, Qsaka Univ.Sch.of Med. Yamadaoka. Suita.Osaka 565.JAPAN.
Application of dexamethasone was found to induce an enhanced expression of mRNA encoding the growth associated protein (GAP-43)after peripheral nerve injury. Following hypoglossal nerve axotomy, a dexamethasone releasing pellet (1.5 mg released in 3 weeks) was placed near the transected nerve. GAP-43 mRNA was detected in the hypoglossal nucleus by non-radioactive in situ hybridization histochemistry using an alkaline phosphatase-labeled oligonucleotide probe.A significant elevation of GAP43mFLNA level was observed 2 weeks after the transection in dexamethasone treated animals. This induction was not observed in the dorsal motor nucleus of vagus which expresses moderately high levels of GAP-43 mFUJA even without nerve injury. Although dexamethasone did not alter the maximum level of GAP-43 mRNA in the hypoglossal nucleus after nerve injury, it prolonged the period in which the mRNA expression remained elevated. This may be due to post-transcriptional effect by the glucocorticoid. Dexamethasone treatment also caused a slight facilitation of reinnervation. This seems due to the enhancement of GAP-43 mRNA level by the glucocorticoid.
1304
c-Fos induction in the superficial dorsal horn by formalin stimulation of the adult rat hindpaw following tibia1 nerve crush Akihiro Yoshidal)z), Hiroyuki Ichikawaz), Tomosada Sugimotoz), Oral and Maxillofacial Surgery II), Oral Anatomy 112), Okayama Uni\ J.Sch. of Dent. Sikata-cho, Okayama, 700, Japan Formalin injection into the hindpaw of rats induces rapid c-Fos expression throughout the 2 days earlier selectively terminal field of the sciatic primary neurons. The tibia1 neurotomy eliminates the c-Fos induction in the medial part of sciatic terminal field (tibia1 territory) and, thereby, enables one to assess the responsiveness of dorsal horn neurons to noxicious primary input through the spared peroneal nerve. When the tibia1 nerve had been crushed 12days before the tibia1 neurotomy, many neurons in the tibia1 territory yielded stimulus-induced c-Fos expression. Therefore, the deafferented dorsal horn neurons in the tibia1 territory responded by c-Fos expression to somatotopically in appropriate (peroneal) primary input. When the nerve had been crushed 19 days before the neurotomy, such ectopic c-Fos inducibility had subsided. The regenerated tibia1 primary neurons were capable of transganglionic transport of WGA-HRP from the hindpaw at 19 days but not 12 days after the nerve crush. Normal dorsal horn somatotopy map is desrupted by a peripheral nerve injury and restored by regeneration.