Effects of beta-amyloid on cholinergic, cholinoceptive and GABAergic neurons

M. Pákáski, Henrietta Papp, Mónika Forgon, P. Kása, B. Penke

Research output: Article

6 Citations (Scopus)

Abstract

Alzheimer's disease is primarily characterized by neurofibrillary tangles, senile plaques and a cholinergic hypofunction. In this study, the morphological signs of toxicity of amyloid β (Aβ) 1-42 and short amyloid peptide fragments corresponding to amino acids 31-35 and 34-39 were investigated on cholinergic, cholinoceptive and GABAergic neuronal populations of basal forebrain cultures. The applied Aβ fragments were toxic to cholinergic, cholinoceptive and GABAergic neurons. In cholinergic and cholinoceptive neurons, the toxic effect caused a redistribution of the acetylcholinesterase within the cells; the characteristic morphological changes in the GABAergic neurons involved the fragmentation and disappearance of the processes. These results suggest that the vulnerability of neurons to Aβ toxicity does not depend on their transmitter content, but the morphological manifestation of this vulnerability differs in the various neuronal populations. The results of experiments with short Aβ fragments led to the conclusion that Leu34 and Met35 may be responsible for the toxicity of amyloid peptides.

Original languageEnglish
Pages (from-to)43-54
Number of pages12
JournalActa Biologica Hungarica
Volume49
Issue number1
Publication statusPublished - 1998

Fingerprint

GABAergic Neurons
Cholinergic Neurons
cholinergic agents
amyloid
Amyloid
Cholinergic Agents
Neurons
Poisons
neurons
toxicity
Toxicity
peptide
vulnerability
Neurofibrillary Tangles
Peptide Fragments
Amyloid Plaques
peptides
Acetylcholinesterase
Population
Alzheimer Disease

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)

Cite this

Effects of beta-amyloid on cholinergic, cholinoceptive and GABAergic neurons. / Pákáski, M.; Papp, Henrietta; Forgon, Mónika; Kása, P.; Penke, B.

In: Acta Biologica Hungarica, Vol. 49, No. 1, 1998, p. 43-54.

Research output: Article

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AU - Papp, Henrietta

AU - Forgon, Mónika

AU - Kása, P.

AU - Penke, B.

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N2 - Alzheimer's disease is primarily characterized by neurofibrillary tangles, senile plaques and a cholinergic hypofunction. In this study, the morphological signs of toxicity of amyloid β (Aβ) 1-42 and short amyloid peptide fragments corresponding to amino acids 31-35 and 34-39 were investigated on cholinergic, cholinoceptive and GABAergic neuronal populations of basal forebrain cultures. The applied Aβ fragments were toxic to cholinergic, cholinoceptive and GABAergic neurons. In cholinergic and cholinoceptive neurons, the toxic effect caused a redistribution of the acetylcholinesterase within the cells; the characteristic morphological changes in the GABAergic neurons involved the fragmentation and disappearance of the processes. These results suggest that the vulnerability of neurons to Aβ toxicity does not depend on their transmitter content, but the morphological manifestation of this vulnerability differs in the various neuronal populations. The results of experiments with short Aβ fragments led to the conclusion that Leu34 and Met35 may be responsible for the toxicity of amyloid peptides.

AB - Alzheimer's disease is primarily characterized by neurofibrillary tangles, senile plaques and a cholinergic hypofunction. In this study, the morphological signs of toxicity of amyloid β (Aβ) 1-42 and short amyloid peptide fragments corresponding to amino acids 31-35 and 34-39 were investigated on cholinergic, cholinoceptive and GABAergic neuronal populations of basal forebrain cultures. The applied Aβ fragments were toxic to cholinergic, cholinoceptive and GABAergic neurons. In cholinergic and cholinoceptive neurons, the toxic effect caused a redistribution of the acetylcholinesterase within the cells; the characteristic morphological changes in the GABAergic neurons involved the fragmentation and disappearance of the processes. These results suggest that the vulnerability of neurons to Aβ toxicity does not depend on their transmitter content, but the morphological manifestation of this vulnerability differs in the various neuronal populations. The results of experiments with short Aβ fragments led to the conclusion that Leu34 and Met35 may be responsible for the toxicity of amyloid peptides.

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KW - GABA immunocytochemistry

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