title: Remodelling sympathetic innervation in rat pancreatic islets ontogeny.
abstract: BACKGROUND
  Pancreatic islets are not fully developed at birth and it is not clear how they are vascularised and innervated. Nerve Growth Factor (NGF) is required to guide sympathetic neurons that innervate peripheral organs and also in cardiovascular system and ovary angiogenesis. Pancreatic beta cells of a transgenic mouse that over-expressed NGF in attracts sympathetic hyper-innervation towards them. Moreover, we have previously demonstrated that adult beta cells synthesize and secrete NGF; however, we do not know how is NGF secreted during development, nor if it might be trophic for sympathetic innervation and survival in the pancreas.We analyzed sympathetic innervation and vasculature development in rat pancreatic islets at different developmental stages; foetal (F19), early postnatal (P1), weaning period (P20) and adults. We temporarily correlated these events to NGF secretion by islet cells.
  
  
  RESULTS
  Sympathetic fibres reached pancreatic islets in the early postnatal period, apparently following blood vessels. The maximal number of sympathetic fibres (TH immunopositive) in the periphery of the islets was observed at P20, and then fibres entered the islets and reached the core where beta cells are mainly located. The number of fibres decreased from that stage to adulthood. At all stages studied, islet cells secreted NGF and also expressed the high affinity receptor TrkA. Foetal and neonatal isolated islet cells secreted more NGF than adults. TrkA receptors were expressed at all stages in pancreatic sympathetic fibres and blood vessels. These last structures were NGF-immunoreactive only at early stages (foetal and P0).
  
  
  CONCLUSIONS
  The results suggest that NGF signalling play an important role in the guidance of blood vessels and sympathetic fibres toward the islets during foetal and neonatal stages and could also preserve innervation at later stages of life.
authors.affiliation: Biophysics Department, Instituto de Fisiología Celular, Neuroscience, Universidad Nacional Autónoma de México, Mexico DF, Mexico. scabrera@ifc.unam.mx
authors.forename: Siraam
authors.initials: S
authors.lastname: Cabrera-Vásquez
authors.forename: Víctor
authors.initials: V
authors.lastname: Navarro-Tableros
authors.forename: Carmen
authors.initials: C
authors.lastname: Sánchez-Soto
authors.forename: Gabriel
authors.initials: G
authors.lastname: Gutiérrez-Ospina
authors.forename: Marcia
authors.initials: M
authors.lastname: Hiriart
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D005260:Female; D005333:Fetus; D005455:Fluorescent Antibody Technique; D018507:Gene Expression Regulation, Developmental; D005934:Glucagon / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000196:embryology / Q000254:growth & development / Q000294:innervation* / Q000378:metabolism; D008297:Male; D018613:Microscopy, Confocal; D008954:Models, Biological; D009414:Nerve Growth Factors / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D020917:Receptor, trkA / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000254:growth & development* / Q000502:physiology*; D014746:Vimentin / Q000378:metabolism
chemical_list: D007328:Insulin; D009414:Nerve Growth Factors; D014746:Vimentin; D005934:Glucagon; D020917:Receptor, trkA