Cellular MTT reduction distinguishes the mechanism of action of β- amyloid from that of tachykinin receptor peptides

Neuropeptides

Volumn 30, Issue 2, 1996, Pages 125-132

  Shearman, M S ^a  

^a NEUROSCIENCE RESEARCH CENTRE   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

2 BENZHYDRYL 3 (2 METHOXYBENZYLAMINO) 1 AZABICYCLO[2.2.2]OCTANE; 2 [1 IMINO 2 (2 METHOXYPHENYL)ETHYL] 7,7 DIPHENYLPERHYDROISOINDOL 4 ONE; 3 (2 METHOXYBENZYLAMINO) 2 PHENYLPIPERIDINE; 3 (4,5 DIMETHYL 2 THIAZOLYL) 2,5 DIPHENYLTETRAZOLIUM BROMIDE; AMYLOID BETA PROTEIN; AMYLOID BETA PROTEIN [25-35]; DYE; KASSININ; NEUROKININ A; SENKTIDE; SPANTIDE; SUBSTANCE P; TACHYKININ RECEPTOR; TACHYKININ RECEPTOR AGONIST; UNCLASSIFIED DRUG;

ANIMAL CELL; ANIMAL TISSUE; ARTICLE; DRUG MECHANISM; DRUG RECEPTOR BINDING; NEUROPATHOLOGY; NEUROTOXICITY; NONHUMAN; OXIDATION REDUCTION REACTION; PEPTIDE ANALYSIS; PHEOCHROMOCYTOMA CELL; PRIORITY JOURNAL; RAT;

ANIMALIA;

EID: 0029945024     PISSN: 01434179     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0143-4179(96)90079-7     Document Type: Article

References (37)

1. Selkoe DJ. The molecular pathology of Alzheimer's disease. Neuron 1991; 6: 487-498.
2. Masters CL, Simms G, Weinman NA, Multhaup G, McDonald BL, Bayreuther K. Amyloid plaque core protein in Alzheimer's disease and Down's syndrome. Proc Natl Acad Sci USA 1985; 82: 4245-4249.
3. Busciglio J, Lorenzo A, Yankner BA. Methodological variables in the assessment of beta-amyloid neurotoxicity. Neurobiol Aging 1992; 13: 609-612.
4. Behl C, Davis J, Cole GM, Schubert D. Vitamin E protects nerve cells from amyloid β protein toxicity. Biochem Biophys Res Commun 1992; 186: 944-950.
5. Pike CJ, Burdick D, Walencewicz AJ, Glabe CG, Cotman CW. Neurodegeneration induced by β-amyloid peptides in vitro: the role of peptide assembly state. J Neurosci 1993; 13: 1676-1687.
6. Mattson MP, Cheng B, Davis D, Bryant K, Lieberburg I, Rydel RE. β-amyloid peptides destabilize calcium homeostasis and render human cortical neurones vulnerable to excitotoxicity. J Neurosci 1992; 12: 376-389.
7. Shearman MS, Ragan CI, Iversen LL. Inhibition of PC12 cell redox activity is a specific, early indicator of the mechanism of β-amyloid-mediated cell death. Proc Natl Acad Sci USA 1994; 91: 1470-1474.
8. Simmons LK, May PC, Tomaselli KJ et al. Secondary structure of amyloid β peptide correlates with neurotoxic activity in vitro. Mol Pharmacol 1994; 45: 373-379.
9. Behl C, Davis JB, Lesley R, Schubert D. Hydrogen peroxide mediates amyloid β protein toxicity. Cell 1994; 77: 817-827.
10. Pike CJ, Walencewicz-Wasserman AJ, Kosmoski J, Cribbs DH, Glabe CG, Cotman C.W. Structure-activity analyses of β-amyloid peptides: contributions of the β25-35 region to aggregation and neurotoxicity. J Neurochem 1995; 64: 253-265.
11. Shearman MS, Hawtin SR, Tailor VJ. The intracellular component of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction is specifically inhibited by β-amyloid peptides. J Neurochem 1995; 65: 218-227.
12. Forloni G, Chiesa R, Smiroldo S et al. Apoptosis mediated neurotoxicity induced by chronic application of β amyloid fragment β25-35. Neuroreport 1993; 4: 523-526.
13. Loo DT, Copani A, Pike CJ, Whittemore ER, Walencewicz AJ, Cotman CW. Apoptosis is induced by β amyloid in cultured nervous system neurones. Proc Natl Acad Sci USA 1993; 90: 7951-7955.
14. Watt JA, Pike CJ, Walencewicz-Wasserman AJ, Cotman CW. Ultrastructural analysis of β-amyloid-induced apoptosis in cultured hippocampal neurons. Brain Res 1994; 661: 147-156.
15. Mussap CJ, Geraghty DP, Burcher E. Tachykinin receptors: a radioligand binding perspective. J Neurochem 1993; 60: 1987-2009.
16. Yankner BA, Duffy LK, Kirschner DA. Neurotrophic and neurotoxic effects of amyloid β protein: reversal by tachykinin neuropeptides. Science 1990; 250: 279-282.
17. Kowall NW, Beal MF, Busciglio J, Duffy LK, Yankner BA. An in vivo model for the neurodegenerative effects of β bamyloid and protection by substance P. Proc Natl Acad Sci USA 1991; 88: 7247-7251.
18. Joslin G, Krause JE, Hershey AD, Adams SP, Fallon RJ, Perlmutter DH. Amyloid-β peptide, substance P, and bombesin bind to the serpin-enzyme complex receptor. J Biol Chem 1991; 266: 21897-21902.
19. Shimohigashi Y, Matsumoto H, Takano Y et al. Receptor-mediated specific biological activity of a β-amyloid protein fragment for NK-1 substance P receptors. Biochem Biophys Res Commun 1993; 193: 624-630.
20. Kimura H, Schubert D. Amyloid β-protein activates tachykinin receptors and inositol trisphosphate accumulation by synergy with glutamate. Proc Natl Acad Sci USA 1993; 90: 7508-7512.
21. Cheung NS, Small DH, Livett BG. An amyloid peptide, βA425-35, mimics the function of substance P on modulation of nicotine-evoked secretion and desensitization in cultured bovine adrenal chromaffin cells. J Neurochem 1993; 60: 1163-1166.
22. Zhao X, Valantas JA, Vyas S, Duffy LK. Comparative toxicity of amyloid β-peptide in neuroblastoma cell lines: effects of albumin and physalaemin. Comp Biochem Physiol 1993; 106: 165-170.
23. 2+ influx in PC12h cells in culture. Neurosci Lett 1994; 173: 147-150.
24. Mitsuhashi M, Akitaya T, Turk C, Payan DG. Amyloid β protein peptides do not interact with the substance P receptor expressed in cultured cells. Mol Brain Res 1991; 11: 177-180.
25. Lee JM, Weinstein DA, Kowall NW, Beal MF. Inability of β-amyloid (25-35) to bind to central nervous system neurokinin 1 receptors. Drug Develop Res 1992; 27: 441-444.
26. Rovero P, Patacchini R, Renzetti AR et al. Interaction of amyloid β protein with tachykinin receptors. Neuropeptides 1992; 22: 99-101.
27. Maggio JE, Stimson ER, Ghilardi JR et al. Reversible in vitro growth of Alzheimer disease β-amyloid plaque by deposition of labeled amyloid peptide. Proc Natl Acad Sci USA 1992; 89: 5462-5466.
28. Burgevin M-C, Daniel N, Double A, Blanchard J-C. The trophic effect of β-amyloid 25-35 peptide is not mediated by NK, or bombesin receptors. Neuroreport 1992; 3: 1131-1134.
29. Joseph R, Han E. Amyloid β-protein fragment 25-35 causes activation of cytoplasmic calcium in neurons. Biochem Biophys Res Commun 1992; 184 1441-1447.
30. May PC, Gitter BD Waters DC et al. β-Amyloid peptide in vitro toxicity: lot-to-lot variability. Neurobiol Aging 1992; 13: 605-608.
31. Di Stefano M, Aleppo G, Casabona G, Genazzani AA, Scapagnini U, Nicoletti F. Amyloid β protein does not interact with tachykinin receptors coupled to inositol phospholipid hydrolysis in human astrocytoma cells. Brain Res 1993; 600: 166-168.
32. Simmons MA, Schneider CR. Amyloid β peptides act directly on single neurons. Neurosci Lett 1993; 150: 133-136.
33. Takadera T, Sakura N, Mohri T, Hashimoto T. Toxic effect of a β-amy oid peptide (β22-35) on the hippocampal neuron and its prevention. Neurosci Lett 1993; 161: 41-44.
34. Ueda K, Fukui Y, Kageyama H. Amyloid β proteininduced neuronal death: neurotoxic properties of aggregated amyloid β protein. Brain Res 1994; 639: 240-244.
35. Klegeris A, Walker DG, McGeer PL. Activation of macrophages by Alzheimer β amyloid peptide. Biochem Biophys Res Commun 1994; 199: 984-991.
36. Frey P, Lis M, Ristig D et al. Studies on the mechanism of β/A4 toxicity. Neurobiol. Aging 1994; 15(S1): S18.
37. Iversen LL, Mortishire-Smith RJ, Pollack SJ, Shearman MS. In vitro toxicity of β-amyloid peptide. Biochem J 1995 (in press).