Vilbig Ryan, Cosmano Jason, Giger Roman, Rochlin M William
Department of Biology, Loyola University Chicago, IL 60626, USA.
J Neurocytol. 2004 Dec;33(6):591-606. doi: 10.1007/s11068-005-3329-8. Epub 2005 Oct 11.
Geniculate ganglion axons arrive in the lingual mesenchyme on embryonic day 13 (E13), 3-4 days before penetrating fungiform papilla epithelium (E17). This latency may result from chemorepulsion by epithelial Sema3A (Dillon et al. (2004) Journal of Comparative Neurology 470, 13-24), or Sema3F, which we report is also expressed in this epithelium. Sema3A and Sema3F repelled or suppressed geniculate neurite outgrowth, respectively, and these effects were stage and neurotrophic factor dependent. BDNF-stimulated outgrowth is repelled by Sema3A until E17, but insensitive to Sema3F from E16. NT-4-stimulated neurite outgrowth is sensitive to Sema3A and Sema3F through E18, but NT-4 has not been detected in E15-18 tongue. E15-18 tongue explants did not exhibit net chemorepulsion of geniculate neurites, but the ability of tongue explants to support geniculate neurite outgrowth fluctuates: E12-13 (Rochlin et al. (2000), Journal of Comparative Neurology, 422, 579-593) and E17-18 explants promote and may attract geniculate neurites, but stages corresponding to intralingual arborization do not. The E18 trophic and tropic effects were evident even in the presence of BDNF or NT-4, suggesting that some other factor is responsible. Intrinsic neurite outgrowth capability (without exogenous neurotrophic factors) fluctuated similarly: ganglia deteriorated at E15, but exhibited moderate outgrowth at E18. The chemorepulsion studies are consistent with a role for Sema3A, not Sema3F, in restricting geniculate axons from the epithelium until E17, when axons penetrate the epithelium. The transient inability of tongue explants to promote geniculate neurite outgrowth may signify an alternative mechanism for restricting geniculate axons from the epithelium: limiting trophic factor access.
膝状神经节轴突在胚胎第13天（E13）到达舌间充质，比穿透菌状乳头上皮（E17）提前3 - 4天。这种延迟可能是由于上皮细胞分泌的Sema3A（狄龙等人，《比较神经学杂志》470卷，13 - 24页，2004年）或Sema3F产生的化学排斥作用导致的，我们报道Sema3F也在该上皮中表达。Sema3A和Sema3F分别排斥或抑制膝状神经突的生长，并且这些作用取决于发育阶段和神经营养因子。BDNF刺激的神经突生长在E17之前受到Sema3A的排斥，但从E16起对Sema3F不敏感。NT - 4刺激的神经突生长在E18之前对Sema3A和Sema3F敏感，但在E15 - 18期的舌组织中未检测到NT - 4。E15 - 18期的舌外植体未表现出对膝状神经突的净化学排斥作用，但舌外植体支持膝状神经突生长的能力存在波动：E12 - 13期（罗奇林等人，《比较神经学杂志》422卷，579 - 593页，2000年）和E17 - 18期的外植体促进并可能吸引膝状神经突，但与舌内分支相对应的阶段则不然。即使存在BDNF或NT - 4，E18期的营养和趋向性效应仍然明显，这表明还有其他一些因子起作用。内在神经突生长能力（无外源性神经营养因子）也有类似的波动：神经节在E15期退化，但在E18期表现出适度的生长。化学排斥研究表明，在E17轴突穿透上皮之前，Sema3A而非Sema3F在限制膝状轴突进入上皮方面发挥作用。舌外植体暂时无法促进膝状神经突生长可能意味着一种限制膝状轴突进入上皮的替代机制：限制神经营养因子的获取。
