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牙髓组织在体外可促进大鼠三叉神经节的神经突生长。

Tooth pulp tissue promotes neurite outgrowth from rat trigeminal ganglia in vitro.

作者信息

Lillesaar C, Eriksson C, Johansson C S, Fried K, Hildebrand C

机构信息

Division of Cell Biology, Department of Biomedicine and Surgery, Faculty of Health Sciences, University of Linköping, Linköping, Sweden.

出版信息

J Neurocytol. 1999 Aug;28(8):663-70. doi: 10.1023/a:1007008815621.

DOI:10.1023/a:1007008815621
PMID:10851345
Abstract

The mammalian tooth pulp becomes innervated by nociceptive and sympathetic axons relatively late during development, when part of the root has formed. In the adult, regenerating axons from an injured tooth nerve or sprouting axons from uninjured nerves in the vicinity rapidly reinnervate denervated tooth pulps. These observations indicate that tooth pulp tissue can use molecular factors to attract pulpal axons from local nerve trunks. The present study examines the hypothesis that these factors include nerve growth factor (NGF), brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF). Explants of trigeminal ganglia from neonatal rat pups showed a distinct neurite outgrowth when co-cultured with pulpal explants collected from molar teeth of 12-day old pups, or after application of a pulpal extract. Control cultures, containing single ganglionic explants, or explants co-cultured with heat-treated pulpal tissue, exhibited a sparse neurite outgrowth. Exogenous NGF and/or GDNF, but not exogenous BDNF, stimulated neurite outgrowth from ganglionic explants. Unexpectedly, application of antibodies against NGF, BDNF and/or GDNF to co-cultures of ganglionic and pulpal explants did not inhibit neuritogenesis. Control experiments showed that IgG molecules readily penetrate the gel used for culture and that even very high concentrations of NGF and GDNF antibodies in combination failed to block neurite growth. On the basis of these data we suggest that other as yet unknown neurite-promoting factors might be present and active in TG/pulpal co-cultures.

摘要

哺乳动物的牙髓在发育过程中相对较晚才被伤害性和交感神经轴突支配,此时牙根的一部分已经形成。在成年动物中,受伤牙神经的再生轴突或附近未受伤神经的发芽轴突会迅速重新支配失神经支配的牙髓。这些观察结果表明,牙髓组织可以利用分子因子从局部神经干吸引牙髓轴突。本研究检验了这样一种假说,即这些因子包括神经生长因子(NGF)、脑源性神经营养因子(BDNF)和胶质细胞系源性神经营养因子(GDNF)。新生大鼠幼崽的三叉神经节外植体与从12日龄幼崽磨牙收集的牙髓外植体共培养时,或在应用牙髓提取物后,显示出明显的神经突生长。对照培养物,包含单个神经节外植体,或与热处理牙髓组织共培养的外植体,显示出稀疏的神经突生长。外源性NGF和/或GDNF,但不是外源性BDNF,刺激神经节外植体的神经突生长。出乎意料的是,将针对NGF、BDNF和/或GDNF的抗体应用于神经节和牙髓外植体的共培养物中,并没有抑制神经突形成。对照实验表明,IgG分子很容易穿透用于培养的凝胶,并且即使是非常高浓度的NGF和GDNF抗体联合使用也未能阻断神经突生长。基于这些数据,我们认为可能存在其他尚未知的促进神经突生长的因子,并在三叉神经节/牙髓共培养物中起作用。

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