Continuous Infusion of β-Amyloid Protein into the Rat Cerebral Ventricle Induces Learning Impairment and Neuronal and Morphological Degeneration
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- Nitta Atsumi NITTA Atsumi
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- Fukuta Taneo FUKUTA Taneo
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- Hasegawa Takaaki [他] HASAGAWA Takaaki
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- NABESIMA Toshitaka
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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Author(s)
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- Nitta Atsumi NITTA Atsumi
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- Fukuta Taneo FUKUTA Taneo
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- Hasegawa Takaaki [他] HASAGAWA Takaaki
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
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- NABESIMA Toshitaka
- Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine
Abstract
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.
Journal
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- The Japanese Journal of Pharmacology
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The Japanese Journal of Pharmacology 73(1), 51-57, 1997-01-01
The Japanese Pharmacological Society
References: 19
-
1
- The presence of heparan sulfate proteoglycans in the neuritic plaques and congophilic angiopathy in Alzheimer's disease
-
SHOW AD.
Am J Pathol 133, 456-463, 1988
Cited by (1)
-
2
- β-Amyloid protein-induced Alzheimer's disease model
-
NITTA A.
Neurosci Lett. 170, 63-66, 1994
Cited by (2)
-
3
- Development of plasticity of brain function with repeated trainings and passage of time after basal forebrain lesions in rats
-
NITTA A.
J Neural Transm [G-sect] 93, 37-46, 1993
Cited by (2)
-
4
- Neuronal dysfunction in rats infused β-amyloid protein into cerebral ventricle
-
ITOH A.
Neurobiol Aging 17, 1996
Cited by (1)
-
5
- In vitro aging of β-amyloid protein causes peptide aggregation and neurotoxicity
-
PIKE CJ.
Brain Res 563, 311-314, 1991
Cited by (3)
-
6
- β-Amyloid peptides destabilize calcium honieostasis and render human cortical neurons vulnerable to excitotoxicity
-
MATTSON MP.
J Neurosci 12, 376-389, 1992
Cited by (1)
-
7
- <no title>
-
MASTERS C. L.
Proc. Natl. Acad. Sci. USA 82, 4245-4249, 1985
DOI Cited by (27)
-
8
- Immunochemical identification of serine protease inhibitor α1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease.
-
ABRAHAM C. A.
Cell 52, 487-501, 1988
Cited by (15)
-
9
- Plaques, tangles and dementia. A quantitative study
-
WILCOCK GK.
J Neurol Sci 56, 343-356, 1982
DOI Cited by (10)
-
10
- Molecular biology of Alzheimer's disease
-
MULLER-HILL B.
Annu Rev Biochem 58, 287-307, 1989
Cited by (2)
-
11
- C. Alzheimer's disease correlation of cortical choline acetyltransferase activity with the severity of deentia and histological abnormalities.
-
WILCOCK GK.
J. Neurol Sci. 57, 407-417, 1982
DOI Cited by (4)
-
12
- <no title>
-
NABESHIMA T.
Tohoku J. Exp. Med. 174, 241-249, 1994
Ichushi Web Cited by (5)
-
13
- Dysfunction of cholinergic and dopaminergic neuronal systems in β-amyloid protein-infused rats
-
ITOH A.
J Neurochem 66, 1113-1117, 1996
Cited by (7)
-
14
- <no title>
-
NABESHIMA T.
Biochem. Biophys. Res. Commun. 175, 215-219, 1991
Cited by (3)
-
15
- <no title>
-
NITTA A.
Eur. J. Pharmacol. 250, 23-30, 1993
Cited by (5)
-
16
- High sensitive assay for choline acetyltransferase activity by high-performance liquid chromatography with electrochemical detection
-
KANEDA N.
Journal of Chromatography 341, 23-30, 1985
DOI Cited by (8)
-
17
- Solvent effects on beta protein toxicity in vivo
-
WAITE J.
Neurobiol Aging 13, 595-599, 1992
DOI Cited by (4)
-
18
- Microsomal metabolism of acetonitrile to cyanide
-
FREEMAN JJ.
Biochem. Pharmacol. 37, 1153-1159, 1988
Cited by (2)
-
19
- N-MethylD-aspartate receptors mediate hypoxic neuronal injury in cortical culture
-
GOLDBERG M. P.
J Pharmacol Exp Ther 243, 784-791, 1987
Cited by (3)
Cited by: 9
-
1
- Molecular Mechanism of Cholinergic Dysfunction and Cognitive Deficits Induced by Amyloid β-Peptide
-
TRAN Manh Hung , YAMADA Kiyofumi , NABESHIMA Toshitaka
日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology 21(4), 125-132, 2001-10-25
Ichushi Web References (71)
-
2
- Effect of NC-1900, and arginine vasopressin derivative, on behavioral impairments in rats with a continuous infusion of β-amyloid protein into the cerebral ventricle [in Japanese]
-
TANAKA Tomoko , YAMADA Kiyofumi , SENZAKI Kouji , KAMEYAMA Tsutomu , NABESHIMA Toshitaka
日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology 17(6), 334, 1997-12-25
Ichushi Web References (2)
-
3
- 柑橘類成分F-1の記憶・学習障害改善作用とそのメカニズム [in Japanese]
-
山國 徹 , 松崎 健太郎 , 大前 直樹 , 平井 学 , 永瀬 弘之 , 井戸 達雄 , TANIA Valdes-Gonzalez , 中川西 修 , 只野 武 , 橋本 道男 , 紫藤 治 , 三巻 祥浩 , 指田 豊 , 大泉 康
応用薬理 69(1), 28-32, 2005-10-01
Ichushi Web References (7)
-
4
- Perspectives of Pharmacotherapy in Alzheimer's Disease
-
YAMADA Kiyofumi , REN Xiuhai , NABESHIMA Toshitaka
The Japanese Journal of Pharmacology 80(1), 9-14, 1999-05-01
J-STAGE Ichushi Web References (30) Cited by (1)
-
5
- Growth Hormone Releaser Attenuates β-Amyloid (1-42)-Induced Memory Impairment in Mice
-
SHIN Eun-Joo , JHOO Jin-Hyeong , NABESHIMA Toshitaka , JHOO Wang-Kee , KWON Myung Sang , LIM Young Kwang , CHAE Jong Seok , JUNG Myung Eun , PARK Seok Joo , JANG Kyung Jin , KIM Hyoung-Chun
Journal of Pharmacological Sciences 99(1), 117-120, 2005-09-20
J-STAGE Ichushi Web References (15) Cited by (1)
-
6
- Aralia cordata Protects Against Amyloid β Protein (25-35)-Induced Neurotoxicity in Cultured Neurons and Has Antidementia Activities in Mice
-
CHO Soon Ock , BAN Jun Yeon , KIM Joo Youn , JEONG Ha Yeon , LEE Ik Soo , SONG Kyung-Sik , BAE KiHwan , SEONG Yeon Hee
Journal of Pharmacological Sciences 111(1), 22-32, 2009-09-20
J-STAGE Ichushi Web References (63) Cited by (2)
-
7
- Pharmacological properties of T-817MA, a novel neurotrophic agent, for treatment of Alzheimer's disease [in Japanese]
-
FUKUSHIMA Tetsuo
Folia Pharmacologica Japonica 136(1), 11-14, 2010-07-01
J-STAGE Ichushi Web References (25)
-
8
- Neuroprotective and Ameliorative Actions of Polyunsaturated Fatty Acids Against Neuronal Diseases : Beneficial Effect of Docosahexaenoic Acid on Cognitive Decline in Alzheimer's Disease
-
HASHIMOTO Michio , HOSSAIN Shahdat
Journal of Pharmacological Sciences 116(2), 150-162, 2011-06-20
J-STAGE Ichushi Web References (122) Cited by (2)
-
9
- TOXICITY OF β-AMYLOID PEPTIDE
-
NABESHIMA Toshitaka , ITOH Akio
The Journal of Toxicological Sciences 23, 177-180, 1998-07-24
J-STAGE Ichushi Web References (17)