Amyloid beta-protein activates tachykinin receptors and inositol trisphosphate accumulation by synergy with glutamate.
- 15 August 1993
- journal article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 90 (16) , 7508-7512
- https://doi.org/10.1073/pnas.90.16.7508
Abstract
The biological function of the soluble form of the amyloid beta-protein (ABP) was examined by assaying its interaction with neuronal receptors expressed in Xenopus oocytes. ABP weakly activated tachykinin receptors, but in the presence of N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methylisoxazole-4- propionate-type glutamate receptors ABP-induced responses were greatly enhanced. Glutamate and ABP together also induced accumulation of inositol trisphosphate and increases in intracellular Ca2+. These observations suggest that in the presence of glutamate, ABP can activate tachykinin receptors and phosphatidylinositol turnover. ABP may therefore act as a neuromodulatory peptide.Keywords
This publication has 34 references indexed in Scilit:
- Release of Excess Amyloid β Protein from a Mutant Amyloid β Protein PrecursorScience, 1993
- Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's diseaseNature, 1991
- An essential role for postsynaptic calmodulin and protein kinase activity in long-term potentiationNature, 1989
- Distribution of protein kinase C-like immunoreactive neurons in rat brainJournal of Neuroscience, 1988
- cDNA eloping of bovine substance-K receptor through oocyte expression systemNature, 1987
- Neurotensin and substance P receptors expressed in Xenopus oocytes by messenger RNA from rat brainProceedings of the Royal Society of London. B. Biological Sciences, 1986
- Regulation of brain Type II Ca2+ calmodulin - dependent protein kinase by autophosphorylation: A Ca2+-triggered molecular switchPublished by Elsevier ,1986
- Regional distribution of type II Ca2+/calmodulin-dependent protein kinase in rat brainJournal of Neuroscience, 1985
- Amyloid plaque core protein in Alzheimer disease and Down syndrome.Proceedings of the National Academy of Sciences, 1985
- Biological evaluation of substance P antagonistsBritish Journal of Pharmacology, 1984