REGULATION OF TASTE GENERATION

味觉为再生的研究提供了一个模型系统， 受体细胞的不断更新及其对 由味觉神经支配。对该项目的研究表明， 几种细胞表面分子在味觉上的差异表达 这种表达依赖于味觉神经支配， 神经纤维第一个具体目标是确定关系 这些分子的表达和味觉细胞类型之间的关系， 这种表达是由支配神经或味觉神经决定的。 上皮 EM免疫细胞化学将解决 NCAM，L1，几种血型抗原，以及其他碳水化合物的味道 细胞类型。 上皮细胞和支配神经的作用 确定味细胞表型将通过表征 在交叉神经支配后， 鼓索（CT）神经或前舌 第九条神经第二个具体目标是确定塑性 孤束核的中枢味觉联系 (NST)在味蕾的去神经支配和神经再支配之后。的 第一个实验将评估CNS对去神经支配的反应。初步 研究表明，味觉神经刺激后， 损伤以及GAP-43的显著组成型表达， NST中的星形胶质细胞和小胶质细胞标记物。这表明， 伴随正常味觉细胞更新的CNS重组。的 终末变性和反应性胶质增生的程度和时间进程 周围神经损伤后，将研究铜-银 变性方法和抗小胶质细胞（OX 42）和星形胶质细胞的抗体 （GFAP）。将使用针对以下的抗体评估再生： 再生轴突（GAP 43和CDA-1）。高尔基体方法将用于 表征味觉神经损伤对NST细胞的影响。第二 一系列的研究将审查终端领域重组 再生的第九神经轴突后（a）第九神经挤压，（B）第九 神经挤压合并膝状体神经节破坏，和（c）交叉- 第IX近端与远端CT吻合。再生纤维将 用HRP标记并映射它们的终端字段。功能研究 将定位响应NST细胞后，上述三个 通过映射c-fos蛋白表达的操作， 第九神经的电刺激和单细胞 来自NST的神经生理学记录响应于味觉， 舌头的触觉和热刺激。

Taste provides a model system for the study of regeneration because of the continual turnover of receptor cells and their trophic dependence on innervation by gustatory nerves. Studies on this project have shown that several cell-surface molecules are differentially expressed on taste cells and that this expression depends upon innervation by gustatory nerve fibers. The first Specific Aim is to determine the relationship between the expression of these molecules and taste cell type and whether this expression is determined by the innervating nerve or the gustatory epithelium. EM immunocytochemistry will address the relation between NCAM, L1, several blood group antigens, and other carbohydrates to taste cell type. The roles of the epithelium and the innervating nerve In determining the taste cell phenotype will be assessed by characterization of vallate and fungiform taste buds following cross-reinnervation of the posterior tongue by the chorda tympani (CT) nerve or the anterior tongue by the IXth nerve. The second Specific Aim is to determine the plasticity of central gustatory connections in the nucleus of the solitary tract (NST) following denervation and reinnervation of the taste buds. The first experiments will assess CNS responses to denervation. Preliminary studies show intense glial reactions in the NST following gustatory nerve injury as well as a significant constitutive expression of GAP-43 and astroglial and microglial markers in the NST. This suggests continual reorganization in the CNS accompanying normal taste cell turnover. The extent and time course of terminal degeneration and reactive gliosis following peripheral nerve injury will be studied by the cupric-silver degeneration method and antibodies against microglia (OX42) and astroglia (GFAP). Regeneration will be assessed using antibodies against regenerating axons (GAP43 and CDA-1). Golgi methods will be used to characterize the effects of taste nerve damage on NST cells. A second series of studies will examine the terminal field reorganization of regenerated IXth nerve axons following (a) IXth nerve crush, (b) IXth nerve crush combined with geniculate ganglion destruction, and (c) cross- anastomosis of proximal IXth to distal CT. Regenerated fibers will be labeled with HRP and their terminal fields mapped. Functional studies will localize responsive NST cells following the above three manipulations by mapping c-fos protein expression in response to electrical stimulation of the IXth nerve and by single-cell neurophysiological recording from the NST in response to gustatory, tactile, and thermal stimulation of the tongue.