Intraventricular administration of the cholinotoxin AF64A increases the accumulation of aluminum in the rat parietal cortex and hippocampus, but not in the frontal cortex

Peter Szerdahelyi, P. Kása

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Aluminum (Al) concentrations of the rat frontal cortex, parietal cortex, and hippocampus were measured by atomic absorption spectroscopy 16 days after a unilateral intracerebroventricular injection of Na gluconate, Al gluconate, or the cholinotoxin AF64A. A fourth group of rats were injected with AF64A 6 days before injection of Al gluconate and subsequently sacrified 10 days later. The combined treatment of AF64A and Al gluconate resulted in enhanced intraneuronal accumulation of Al in the parietal cortex and hippocampus but not in the frontal cortex. Consequently, Al may not be considered to be a primary factor in the pathogenesis of Alzheimer's disease.

Original languageEnglish
Pages (from-to)356-360
Number of pages5
JournalBrain Research
Volume444
Issue number2
DOIs
Publication statusPublished - Mar 22 1988

Fingerprint

Parietal Lobe
Frontal Lobe
Aluminum
Hippocampus
Injections
ethylcholine aziridinium
Spectrum Analysis
Alzheimer Disease
gluconic acid

Keywords

  • Aluminum accumulation
  • Alzheimer's disease
  • Cholinotoxin (AF64A)
  • Hippocampus
  • Parietal cortex
  • Rat brain
  • Regional difference

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

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abstract = "Aluminum (Al) concentrations of the rat frontal cortex, parietal cortex, and hippocampus were measured by atomic absorption spectroscopy 16 days after a unilateral intracerebroventricular injection of Na gluconate, Al gluconate, or the cholinotoxin AF64A. A fourth group of rats were injected with AF64A 6 days before injection of Al gluconate and subsequently sacrified 10 days later. The combined treatment of AF64A and Al gluconate resulted in enhanced intraneuronal accumulation of Al in the parietal cortex and hippocampus but not in the frontal cortex. Consequently, Al may not be considered to be a primary factor in the pathogenesis of Alzheimer's disease.",
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