| Literature DB >> 8581496 |
T Harkany1, G I De Jong, K Soós, B Penke, P G Luiten, K Gulya.
Abstract
beta-Amyloid(1-42) peptide (beta AP(1-42) was injected into the medial septum of rats. After a 14-day survival time, neuronal alterations in the septal cholinergic and GABAergic systems were visualized by means of histo- and immunocytochemical methods. Neurons insulted by the peptide were primary choline acetyltransferase-immunoreactive (ir), while only minor effects of beta AP(1-42) were observed on parvalbumin-ir interneurons. These results indicate that the changes in intracellular Ca2+ level elicited by beta AP(1-42) may contribute to beta-amyloid neurotoxicity, and Ca(2+)-binding proteins may play an important role in the protection against the neurotoxic effects of beta AP(1-42).Entities:
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Year: 1995 PMID: 8581496 DOI: 10.1016/0006-8993(95)01013-l
Source DB: PubMed Journal: Brain Res ISSN: 0006-8993 Impact factor: 3.252