Growth-associated protein-43 (GAP-43) in the regenerating periodontal Ruffini endings of the rat incisor following injury to the inferior alveolar nerve
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Youn, SH
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机构:Osaka Univ, Fac Dent, Dept Oral Anat & Dev Biol, Suita, Osaka 5650871, Japan
Youn, SH
Maeda, T
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机构:Osaka Univ, Fac Dent, Dept Oral Anat & Dev Biol, Suita, Osaka 5650871, Japan
Maeda, T
Kurisu, K
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机构:Osaka Univ, Fac Dent, Dept Oral Anat & Dev Biol, Suita, Osaka 5650871, Japan
Kurisu, K
Wakisaka, S
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机构:Osaka Univ, Fac Dent, Dept Oral Anat & Dev Biol, Suita, Osaka 5650871, Japan
Wakisaka, S
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[1] Osaka Univ, Fac Dent, Dept Oral Anat & Dev Biol, Suita, Osaka 5650871, Japan
[2] Niigata Univ, Sch Dent, Dept Oral Anat, Niigata, Japan
Alterations in the levels of growth-associated protein 43 (GAP-43)-like immunoreactivity (-LI) were examined in the lingual periodontal ligament of the rat incisor following two types of injury (resection and crush) to the inferior alveolar nerve (IAN). In normal animals, GAP-43-like immunoreactive (IR) structures were observed as tree-like ramifications in the alveolar half of the lingual periodontal ligament of incisors. Under immunoelectron microscopy, GAP-43-LI appeared in the Schwann sheaths associated with periodontal Ruffini endings; neither cell bodies of the terminal Schwann cells nor axonal profiles showed CAP-43-LI. During regeneration of the periodontal Ruffini endings following resection of the IAN, GAP-43-LI appeared in the cytoplasm of the terminal Schwann cell bodies and axoplasm of the terminals. The distribution of GAP-43-LI in the Ruffini endings returned to almost normal levels on days 28 and 56 following the injury. The changes in the distribution of GAP-43-LI following the crush injury were similar to those following resection; however, expression of GAP-43-LI was slightly higher for the entire experimental period compared with the resection. The transient expression of GAP-43 in the terminal Schwann cells and axonal profiles of the periodontal Ruffini endings following nerve injury suggests that GAP-43 is closely associated with axon-schwann cells interactions during regeneration. (C) 1998 Elsevier Science B.V.