Abstract：
:We previously reported that the amyloid-beta protein (Abeta) reduces the synthesis of acetylcholine (ACh) in a mouse septal cell line, SN56, without causing death of the cells. Here, we report that the ACh-reducing effect of either Abeta 1-28 or Abeta 1-42 (100 nM; 48 h) in SN56 cells can be prevented by a co-treatment with the tyrosine kinase inhibitors, genistein (75 microM) and tyrphostin A25 (50 microM). Treatment of the cells with either of these inhibitors alone increased ACh levels. An enhancement of the cellular ACh content was also obtained with aphidicolin, a compound which inhibits DNA synthesis. However, co-treatment of the cells for 48 h with aphidicolin (500 nM) and Abeta 1-42 (100 nM) did not prevent the reduction in ACh levels caused by the peptide. Furthermore, this effect could not prevented by a pre-treatment with vitamin E (50 microg/ml). These results suggest that the ACh-reducing effect of Abeta in SN56 cells is dependent on tyrosine phosphorylation, but is not dependent on DNA synthesis and may not be mediated by free radicals.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Pedersen WA,Blusztajn JKdoi
10.1016/s0304-3940(97)00913-0subject
Has Abstractpub_date
1997-12-19 00:00:00pages
77-80issue
2-3eissn
0304-3940issn
1872-7972pii
S0304-3940(97)00913-0journal_volume
239pub_type
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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