Experimental techniques for developing new drugs acting on dementia (10) Alzheimer's disease animal model induced by β-amyloid protein

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

To develop an animal model of Alzheimer's disease, β-amyloid protein was infused into the rat cerebral ventricle for 14 days using a mini-osmotic pump. The performance of some memory tasks in the β-amyloid protein-treated rats was impaired. Long-term potentiation in the hippocampus was impaired in β-amyloid-infused rats. The impairment of memory under the infusion could be recovered by two cognitive enhancer drugs. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus but glial fibrillary acidic protein immunoreactivity increased in the cortex both immediately and 2 weeks after cessation of the infusion. Ciliary neurotrophic factor contents in several brain areas in β-amyloid-infused rat significantly increased. Substance P and microtubule-associated protein, which play an important role in neuronal transmission and construction of neuronal cells, respectively decreased. Moreover, the release of acetylcholine and dopamine from the cortex/hippocampus and striatum, respectively, in the β-amyloid-infused rats after depolarization was smaller than that from the control rats. These results suggest that β-amyloid protein induced dysfunction of the central nervous system in vivo, and that the animal could be used as a model of Alzheimer's disease.

Original languageEnglish
Pages (from-to)85-90
Number of pages6
JournalJapanese Journal of Psychopharmacology
Volume16
Issue number3
Publication statusPublished - 11-09-1996
Externally publishedYes

Fingerprint

Amyloidogenic Proteins
Animal Disease Models
Alzheimer Disease
Amyloid
Pharmaceutical Preparations
Hippocampus
Ciliary Neurotrophic Factor
Nootropic Agents
Cerebral Ventricles
Microtubule-Associated Proteins
Choline O-Acetyltransferase
Long-Term Potentiation
Glial Fibrillary Acidic Protein
Frontal Lobe
Substance P
Acetylcholine
Dopamine
Central Nervous System
Animal Models
Brain

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

@article{c9f86ca0680d4b3489ff726ed2b660b4,
title = "Experimental techniques for developing new drugs acting on dementia (10) Alzheimer's disease animal model induced by β-amyloid protein",
abstract = "To develop an animal model of Alzheimer's disease, β-amyloid protein was infused into the rat cerebral ventricle for 14 days using a mini-osmotic pump. The performance of some memory tasks in the β-amyloid protein-treated rats was impaired. Long-term potentiation in the hippocampus was impaired in β-amyloid-infused rats. The impairment of memory under the infusion could be recovered by two cognitive enhancer drugs. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus but glial fibrillary acidic protein immunoreactivity increased in the cortex both immediately and 2 weeks after cessation of the infusion. Ciliary neurotrophic factor contents in several brain areas in β-amyloid-infused rat significantly increased. Substance P and microtubule-associated protein, which play an important role in neuronal transmission and construction of neuronal cells, respectively decreased. Moreover, the release of acetylcholine and dopamine from the cortex/hippocampus and striatum, respectively, in the β-amyloid-infused rats after depolarization was smaller than that from the control rats. These results suggest that β-amyloid protein induced dysfunction of the central nervous system in vivo, and that the animal could be used as a model of Alzheimer's disease.",
author = "A. Nitta and Toshitaka Nabeshima",
year = "1996",
month = "9",
day = "11",
language = "English",
volume = "16",
pages = "85--90",
journal = "Neuropsychopharmacology Reports",
issn = "1340-2544",
publisher = "John Wiley and Sons Inc.",
number = "3",

}

TY - JOUR

T1 - Experimental techniques for developing new drugs acting on dementia (10) Alzheimer's disease animal model induced by β-amyloid protein

AU - Nitta, A.

AU - Nabeshima, Toshitaka

PY - 1996/9/11

Y1 - 1996/9/11

N2 - To develop an animal model of Alzheimer's disease, β-amyloid protein was infused into the rat cerebral ventricle for 14 days using a mini-osmotic pump. The performance of some memory tasks in the β-amyloid protein-treated rats was impaired. Long-term potentiation in the hippocampus was impaired in β-amyloid-infused rats. The impairment of memory under the infusion could be recovered by two cognitive enhancer drugs. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus but glial fibrillary acidic protein immunoreactivity increased in the cortex both immediately and 2 weeks after cessation of the infusion. Ciliary neurotrophic factor contents in several brain areas in β-amyloid-infused rat significantly increased. Substance P and microtubule-associated protein, which play an important role in neuronal transmission and construction of neuronal cells, respectively decreased. Moreover, the release of acetylcholine and dopamine from the cortex/hippocampus and striatum, respectively, in the β-amyloid-infused rats after depolarization was smaller than that from the control rats. These results suggest that β-amyloid protein induced dysfunction of the central nervous system in vivo, and that the animal could be used as a model of Alzheimer's disease.

AB - To develop an animal model of Alzheimer's disease, β-amyloid protein was infused into the rat cerebral ventricle for 14 days using a mini-osmotic pump. The performance of some memory tasks in the β-amyloid protein-treated rats was impaired. Long-term potentiation in the hippocampus was impaired in β-amyloid-infused rats. The impairment of memory under the infusion could be recovered by two cognitive enhancer drugs. Choline acetyltransferase activity significantly decreased in the frontal cortex and hippocampus but glial fibrillary acidic protein immunoreactivity increased in the cortex both immediately and 2 weeks after cessation of the infusion. Ciliary neurotrophic factor contents in several brain areas in β-amyloid-infused rat significantly increased. Substance P and microtubule-associated protein, which play an important role in neuronal transmission and construction of neuronal cells, respectively decreased. Moreover, the release of acetylcholine and dopamine from the cortex/hippocampus and striatum, respectively, in the β-amyloid-infused rats after depolarization was smaller than that from the control rats. These results suggest that β-amyloid protein induced dysfunction of the central nervous system in vivo, and that the animal could be used as a model of Alzheimer's disease.

UR - http://www.scopus.com/inward/record.url?scp=0029848494&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029848494&partnerID=8YFLogxK

M3 - Article

C2 - 8905795

AN - SCOPUS:0029848494

VL - 16

SP - 85

EP - 90

JO - Neuropsychopharmacology Reports

JF - Neuropsychopharmacology Reports

SN - 1340-2544

IS - 3

ER -