Long-term deprivation of oestrogens by ovariectomy potentiates β-amyloid-induced working memory deficits in rats

Kiyofumi Yamada, Tomoko Tanaka, Li Bo Zou, Kouji Senzaki, Kohji Yano, Takashi Osada, Olariu Ana, Xiuhai Ren, Tsutomu Kameyama, Toshitaka Nabeshima

Research output: Contribution to journalArticle

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Abstract

1. In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory deficits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid β-peptide (Aβ), the major constituent of senile plaques in AD. 2. Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a significant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3. A continuous i.c.v. infusion of Aβ-(1-42) caused spatial learning and memory deficits in both ovariectomized and sham-operated rats. 4. The Aβ-induced working memory deficits were significantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5. These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory deficits produced by Aβ-(1-42) in rats.

Original languageEnglish
Pages (from-to)419-427
Number of pages9
JournalBritish Journal of Pharmacology
Volume128
Issue number2
DOIs
Publication statusPublished - 11-10-1999

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Memory Disorders
Ovariectomy
Short-Term Memory
Amyloid
Estrogens
Intraventricular Infusions
Aptitude
Amyloid Plaques
Learning
Water
Spatial Memory
Spatial Learning

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Yamada, Kiyofumi ; Tanaka, Tomoko ; Zou, Li Bo ; Senzaki, Kouji ; Yano, Kohji ; Osada, Takashi ; Ana, Olariu ; Ren, Xiuhai ; Kameyama, Tsutomu ; Nabeshima, Toshitaka. / Long-term deprivation of oestrogens by ovariectomy potentiates β-amyloid-induced working memory deficits in rats. In: British Journal of Pharmacology. 1999 ; Vol. 128, No. 2. pp. 419-427.
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abstract = "1. In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory deficits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid β-peptide (Aβ), the major constituent of senile plaques in AD. 2. Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a significant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3. A continuous i.c.v. infusion of Aβ-(1-42) caused spatial learning and memory deficits in both ovariectomized and sham-operated rats. 4. The Aβ-induced working memory deficits were significantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5. These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory deficits produced by Aβ-(1-42) in rats.",
author = "Kiyofumi Yamada and Tomoko Tanaka and Zou, {Li Bo} and Kouji Senzaki and Kohji Yano and Takashi Osada and Olariu Ana and Xiuhai Ren and Tsutomu Kameyama and Toshitaka Nabeshima",
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Yamada, K, Tanaka, T, Zou, LB, Senzaki, K, Yano, K, Osada, T, Ana, O, Ren, X, Kameyama, T & Nabeshima, T 1999, 'Long-term deprivation of oestrogens by ovariectomy potentiates β-amyloid-induced working memory deficits in rats', British Journal of Pharmacology, vol. 128, no. 2, pp. 419-427. https://doi.org/10.1038/sj.bjp.0702811

Long-term deprivation of oestrogens by ovariectomy potentiates β-amyloid-induced working memory deficits in rats. / Yamada, Kiyofumi; Tanaka, Tomoko; Zou, Li Bo; Senzaki, Kouji; Yano, Kohji; Osada, Takashi; Ana, Olariu; Ren, Xiuhai; Kameyama, Tsutomu; Nabeshima, Toshitaka.

In: British Journal of Pharmacology, Vol. 128, No. 2, 11.10.1999, p. 419-427.

Research output: Contribution to journalArticle

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AU - Yamada, Kiyofumi

AU - Tanaka, Tomoko

AU - Zou, Li Bo

AU - Senzaki, Kouji

AU - Yano, Kohji

AU - Osada, Takashi

AU - Ana, Olariu

AU - Ren, Xiuhai

AU - Kameyama, Tsutomu

AU - Nabeshima, Toshitaka

PY - 1999/10/11

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N2 - 1. In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory deficits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid β-peptide (Aβ), the major constituent of senile plaques in AD. 2. Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a significant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3. A continuous i.c.v. infusion of Aβ-(1-42) caused spatial learning and memory deficits in both ovariectomized and sham-operated rats. 4. The Aβ-induced working memory deficits were significantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5. These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory deficits produced by Aβ-(1-42) in rats.

AB - 1. In the present study, we examined whether deprivation of oestrogens by ovariectomy could modify learning and memory deficits caused by a continuous intracerebroventricular (i.c.v.) infusion of amyloid β-peptide (Aβ), the major constituent of senile plaques in AD. 2. Neither long-term (3 months) nor short-term (1 month), deprivation of oestrogens by ovariectomy caused a significant impairment in spatial learning and memory in a water maze and spontaneous alternation behaviour in a Y-maze. 3. A continuous i.c.v. infusion of Aβ-(1-42) caused spatial learning and memory deficits in both ovariectomized and sham-operated rats. 4. The Aβ-induced working memory deficits were significantly potentiated in ovariectomized rats compared with sham-operated rats when mnemonic ability was examined 3 months after ovariectomy. 5. These results suggest that long-term deprivation of oestrogens induced by ovariectomy increases susceptibility to memory deficits produced by Aβ-(1-42) in rats.

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