Premium
Amyloid β peptide is not a candidate for the neurotrophic activities released from chromaffin cells
Author(s) -
Legutko Beata,
Staufenbiel Matthias,
Krieglstein Kerstin
Publication year - 1998
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/s0736-5748(98)00037-9
Subject(s) - adrenal medulla , embryonic stem cell , hippocampal formation , biology , microbiology and biotechnology , amyloid beta , neurotrophin , central nervous system , neuron , neuroscience , amyloid (mycology) , beta (programming language) , medicine , peptide , endocrinology , biochemistry , catecholamine , botany , receptor , gene , computer science , programming language
We have previously shown that chromaffin cells, the neuron‐like cells of the adrenal medulla, release proteins, which promote in vitro survival of a large number of peripheral and central nervous system neurons (cf. Lachmund, A., Gehrke, D., Krieglstein, K. and Unsicker, K, Trophic factors from chromaffin granules promote survival of peripheral and central nervous system neurons. Neuroscience , 1994, 62, 361–370). In a search for the active molecules we are testing compounds that are known to be synthesized and released by chromaffin cells. Amyloid precursor protein ( β APP) is one of these factors (Bieger, S., Klafki, H.‐W. and Unsicker, K., Synthesis and release of the β ‐amyloid precursor protein by bovine chromaffin cells. Neurosci. Lett. , 1993, 162, 173–175). In the present study we have investigated the possibility that amyloid β peptide (A β P) generated from β APP may have survival supporting effects for neurons from embryonic chick ciliary (CG) and dorsal root ganglia (DRG). Embryonic rat hippocampal neurons, for which promotion of short‐term survival by A β P has been reported (Whitson, J. S., Selkoe, D. J. and Cotman, C. W., Amyloid β protein enhances the survival of hippocampal neurons in vitro. Science , 1989, 243, 1488–1490), were employed as a reference. A β P fragment 1–40, administered over a wide range of concentrations (1.5–100 μ mg\ml) did not promote the survival of CG and DRG neurons isolated from embryonic day (E) 8 chick embryos. The peptide also failed to toxically suppress survival of these neuron populations in the presence of survival promoting factors. In confirmation of previous reports, the 1–40 peptide, in comparison to the reverse 40–1 peptide, significantly enhanced survival of hippocampal neurons. These results suggest that A β P is not a trophic factor for the peripheral neuron populations tested and, most likely, not a neurotrophic component among the neurotrophic factors released by chromaffin cells.