Neuronal vs. glial somatostatin in the hypothalamus: a cell culture study of the ontogenesis of cellular location, content and release.
Somatostatin (SRIH) is an ubiquitous peptide subserving functions as a hypothalamic-hypophysial regulatory peptide and as a neuromodulator in the CNS, as well as various roles in the periphery. Based on our earlier observations that the ability of primary cultures of foetal rat hypothalamic cells to secrete SRIH developed distinct differences depending on whether they were maintained in a serum-supplemented medium (SSM) or a defined, serum free medium (DM), coupled with recent reports that glia in several brain regions may express neuropeptides, we have investigated the cellular location of SRIH in these cultures. Using immunocytochemical techniques (ICC) for the simultaneous location of SRIH and glial fibrillary acidic protein (GFAP) we found that SRIH-like immunoreactivity (SRIH-LI) was present in a significant number of hypothalamic glial cells around the time of birth. In the presence of serum, this expression persists and even by day 9 in culture a dense and intense immunofluorescent SRIH-LI signal was observed in GFAP positive cells. However, in DM glial expression is switched off rapidly (although GFAP positive cells are still present) until SRIH-LI eventually occurs at a much reduced abundance in GFAP negative neuronal cell types. In addition, the SRIH content of SSM cultures was three-fold greater than that from SSM cultures. Thus our results indicate that the mechanisms for SRIH-LI release from astrocytes appears to be distinctly different to that from neuronal-type cells. We propose that glial cell expression of SRIH-LI may represent a developmentally important phenomenon in the hypothalamus, e.g. serving a trophic role during critical times of development, and that its expression in glia may be stimulated by factors present in serum. Consequently, an understanding of factors which regulate SRIH expression and release from glia is likely to be of importance to our understanding of brain development, injury, repair and diseases of the CNS.
Davidson
K
K
Department of Pharmacology, Charing Cross and Westminster Medical School, London, UK.
Gillies
G E
GE
D000818:Animals; D002478:Cells, Cultured; D003470:Culture Media; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007031:Hypothalamus / Q000166:cytology / Q000378:metabolism*; D007150:Immunohistochemistry; D009457:Neuroglia / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D013004:Somatostatin / Q000378:metabolism*; D014018:Tissue Distribution
D003470:Culture Media; D005904:Glial Fibrillary Acidic Protein; D013004:Somatostatin