Aged synthetic human amyloid β-peptide 1-42 and related fragments induce direct acetylcholine release from rat basal forebrain tissue slices

Mónika Forgon, Z. Farkas, Magdolna Pákáski, Márta Zarándi, B. Penke

Research output: Contribution to journalArticle

Abstract

The direct effects of synthetic human amyloid β-peptide 1-42 (Aβ1-42), scrambled Aβ1-42 (MODI and MOD2), and related fragments (Aβ31-35, Aβ34-39, and Aβ17-21), either freshly dissolved (non-aged) or aged for 2, 4, 12 and 24 h, were studied on acetylcholine release from rat basal forebrain tissue slices. In in vitro tissue slices, Aβ1-42 aged for 2 h, and Aβ31-35 and Aβ34-39 aged for 24 h evoked acetylcholine release from the basal forebrain tissue slices in a Ca2+-dependent manner. Transmitter release was not observed on the use of freshly dissolved Aβ1-42 and scrambled Aβ1-42 (MODI and MOD2) and Aβ17-21 aged for 24 h. These data support the suggestion that it is the fibrillar (aggregated) form which is effective on the axon terminals and evokes direct acetylcholine release. It is proposed that one of the roles of Aβ in the brain is the presynaptic modulation of acetylcholine release, in this way causing first an altered Ca2+-homeostasis, then cholinergic hypoactivity and finally the retrograde degenaration of cholinergic nerve cells.

Original languageEnglish
Pages (from-to)71-78
Number of pages8
JournalActa biologica Hungarica
Volume49
Issue number1
Publication statusPublished - Dec 1 1998

Keywords

  • Acetylcholine release
  • Aggregation
  • Alzheimer's disease
  • Amyloid β-peptide
  • Basal forebrain
  • Tissue slices

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Environmental Science(all)
  • Neurology

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