Continuous Infusion of β-Amyloid Protein into the Rat Cerebral Ventricle Induces Learning Impairment and Neuronal and Morphological Degeneration

• Published in: Japanese journal of pharmacology Vol. 73; no. 1; pp. 51 - 57
• Main Authors: Nitta, Atsumi, Fukuta, Taneo, Hasegawa, Takaaki, Nabeshima, Toshitaka
• Format: Journal Article
• Language: English
• Published: Japan 01.01.1997
• Subjects: Alzheimer’s disease; Amyloid beta-Peptides - toxicity; Amyloid protein; Animals; Avoidance Learning - drug effects; Choline O-Acetyltransferase - antagonists & inhibitors; Cholinergic neuron; Corpus Striatum - drug effects; Corpus Striatum - enzymology; Frontal Lobe - drug effects; Frontal Lobe - enzymology; Glial fibrillary acidic protein; Glial Fibrillary Acidic Protein - analysis; Hippocampus - drug effects; Hippocampus - enzymology; Hippocampus - ultrastructure; Immunohistochemistry; Injections, Intraventricular; Learning and memory; Male; Maze Learning - drug effects; Nerve Degeneration - drug effects; Parietal Lobe - drug effects; Parietal Lobe - enzymology; Rats; Rats, Wistar; Learning and memory; Cholinergic neuron; Alzheimer’s disease; Amyloid protein; Glial fibrillary acidic protein
• DOI: 10.1254/jjp.60.51
• ISSN: 0021-5198

To investigate the toxicity of β-amyloid protein, a component of the senile plaques in Alzheimer’s disease, it was infused into the cerebral ventricle of rats for 14 days by a mini-osmotic pump. Performances in the water maze and passive avoidance tasks in β-amyloid protein-treated rats were impaired. Choline acetyltransferase activity significantly decreased in the hippocampus both immediately and 2 weeks after the cessation of the infusion. However, the learning impairment was recoverable 2 weeks after cessation of the infusion. Both immediately and 2 weeks after the cessation of the infusion, glial fibrillary acidic protein immunoreactivity increased. Furthermore, β-amyloid protein altered the staining in the nuclei of hippocampal cells for only 2 weeks after the cessation. These results suggest that β-amyloid protein produces some damage in the central nervous system in vivo.