In vivo presence of the high affinity nerve growth factor receptor Trk-A in the rat pancreas: differential localization during pancreatic development.

It is now established that the pancreatic islet cells derive from precursors present in the pancreatic ducts. These precursor cells as well as the factors that influence their differentiation to mature insulin-secreting beta-islet cells are nevertheless not elucidated yet. However, the large number of similarities existing between beta-cells and neuronal cells led to the suggestion that these two different cell types may be sensitive to the same growth and differentiation factors, for example, nerve growth factor (NGF), which is important for the differentiation and survival of several neurons. It was previously demonstrated that the high affinity NGF receptor, Trk-A, which is sufficient for NGF signal transduction, is expressed in different beta-cell lines and in normal rat islet cells in primary culture. The aim of this study was therefore to examine whether the Trk-A receptor is present in vivo in the rat pancreas during development and in adult life. By double immunofluorescence analysis using anti-Trk-A/antiinsulin or anti-Trk-A/antiglucagon antibodies on pancreatic sections of adult rats, it is demonstrated that the Trk-A protein is present in the beta- and not in the alpha-islet cells of adult rat pancreas. No Trk-A immunostaining was observed in the exocrine pancreas or in the pancreatic ducts of adult pancreas. Interestingly, the pattern of Trk-A immunolocalization in the pancreas is different during fetal life, when Trk-A immunostaining is observed in the pancreatic ductular cells and undetectable in both beta- and alpha-islet cells. During late prenatal and early postnatal life, Trk-A immunostaining is present in the islet cells, although weaker than in adult rats, and progressively decreases in the pancreatic ducts, as pancreatic maturation progresses. The intensity and localization of the Trk-A immunostaining in the rat pancreas are therefore developmentally regulated.