Abstract
The insulin‐like growth factor (IGF) system is an important regulator of growth and differentiation in a variety of tissues. In the present study, the expression of IGF family members in the taste buds of mice and rats was examined. By reverse transcriptase polymerase chain reaction (RT‐PCR) analysis, mRNA of IGF‐I and ‐II, IGF‐I receptor (IGF‐IR), insulin receptor (insulin R), and IGF‐binding protein (IGFBP)‐2, ‐3, ‐4, ‐5, and ‐6 was detected in the taste bud‐containing epithelium of the circumvallate papillae of mice. As suggested by the study using degenerate PCR (McLaughlin [2000] J. Neurosci. 20:5679–5688), IGF‐IR was expressed in most of the taste bud cells of adult mice, as found by immunohistochemistry, and in those of postnatal day (P) 6 mice by in situ hybridization. Insulin R, which has strong homology to IGF‐IR, was also detected in most of the taste bud cells of mice by immunohistochemistry and in situ hybridization. IGF‐I immunoreactivity was detected in a few taste bud cells and in the epithelium surrounding taste buds. Northern blot analysis revealed that the amount of IGF‐I mRNA in taste bud‐containing epithelium was very low compared with that in liver. IGF‐II immunoreactivity was weakly detected in mouse taste buds and the surrounding epithelium. In the rat tissue, a subset of the taste bud cells was positive for IGF‐II. Among the six IGFBPs, IGFBP‐2, ‐5, and ‐6 were detected in the mouse taste buds: IGFBP‐2 and ‐5 immunoreactivity was seen in the majority of the taste bud cells, whereas IGFBP‐6 immunoreactivity was found in the nerve fibers innervating the taste buds. In situ hybridization study also revealed that IGFBP‐2 and ‐5 mRNA was synthesized in the taste buds of P6 mice and that the expression of these mRNAs overlapped in von Ebner's glands. These data reveal that IGF‐I and ‐II might be produced in taste bud cells and (or) surrounding lingual epithelium and act through IGF‐IR and insulin R locally in a paracrine and autocrine manner. The activity of these IGFs may be modulated through their interaction with IGFBP‐2, ‐5, and 6. J. Comp. Neurol. 482:74–84, 2005. © 2004 Wiley‐Liss, Inc.