Ethanol withdrawal-induced impaired recognition is reversed by chronic exposure to stress and the acute administration of corticosterone in mice

Hideaki Kato, Minoru Tsuji, Kazuya Miyagawa, Kotaro Takeda, Hiroshi Takeda

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

The present study was designed to ascertain the effects of repeated exposure to stress and the acute administration of corticosterone (1, 3, 10 mg/kg, intraperitoneally (i.p.)) on the ethanol withdrawal-induced impairment of novel object recognition in mice. Mice were chronically treated with 3% ethanol for 7 d, with or without exposure to restraint stress for 1 h/d. A significant decrease in cognitive function was observed in the ethanol plus no stress group at 48 h after the discontinuation of ethanol treatment. This impaired recognition was recovered in the ethanol plus stress group. Moreover, we investigated the effects of acute pretreatment with corticosterone, which is a corticosteroid-type hormone produced in the cortex of the adrenal glands, on the impaired recognition after the discontinuation of ethanol treatment in mice. The impaired recognition in the 3% ethanol alone-treated group at 48 h after the discontinuation of ethanol treatment was recovered by treatment with the middle dose (3 mg/kg) of corticosterone, but not with the low or high doses (1, 10 mg/kg). These results suggest that chronic stress during the development of ethanol dependence may reduce the impaired recognition after the discontinuation of ethanol treatment. Moreover, acute pretreatment with the middle dose of corticosterone also recovered the impaired recognition after the discontinuation of ethanol treatment in mice. Adequate regulation of the hypothalamic-pituitary-adrenal (HPA) axis by corticosterone may improve the impaired recognition after the discontinuation of ethanol treatment.

Original languageEnglish
Pages (from-to)1631-1637
Number of pages7
JournalBiological and Pharmaceutical Bulletin
Volume39
Issue number10
DOIs
Publication statusPublished - 01-01-2016

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Corticosterone
Ethanol
Recognition (Psychology)
Adrenal Glands
Cognition
Adrenal Cortex Hormones
Hormones

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmaceutical Science

Cite this

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abstract = "The present study was designed to ascertain the effects of repeated exposure to stress and the acute administration of corticosterone (1, 3, 10 mg/kg, intraperitoneally (i.p.)) on the ethanol withdrawal-induced impairment of novel object recognition in mice. Mice were chronically treated with 3{\%} ethanol for 7 d, with or without exposure to restraint stress for 1 h/d. A significant decrease in cognitive function was observed in the ethanol plus no stress group at 48 h after the discontinuation of ethanol treatment. This impaired recognition was recovered in the ethanol plus stress group. Moreover, we investigated the effects of acute pretreatment with corticosterone, which is a corticosteroid-type hormone produced in the cortex of the adrenal glands, on the impaired recognition after the discontinuation of ethanol treatment in mice. The impaired recognition in the 3{\%} ethanol alone-treated group at 48 h after the discontinuation of ethanol treatment was recovered by treatment with the middle dose (3 mg/kg) of corticosterone, but not with the low or high doses (1, 10 mg/kg). These results suggest that chronic stress during the development of ethanol dependence may reduce the impaired recognition after the discontinuation of ethanol treatment. Moreover, acute pretreatment with the middle dose of corticosterone also recovered the impaired recognition after the discontinuation of ethanol treatment in mice. Adequate regulation of the hypothalamic-pituitary-adrenal (HPA) axis by corticosterone may improve the impaired recognition after the discontinuation of ethanol treatment.",
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Ethanol withdrawal-induced impaired recognition is reversed by chronic exposure to stress and the acute administration of corticosterone in mice. / Kato, Hideaki; Tsuji, Minoru; Miyagawa, Kazuya; Takeda, Kotaro; Takeda, Hiroshi.

In: Biological and Pharmaceutical Bulletin, Vol. 39, No. 10, 01.01.2016, p. 1631-1637.

Research output: Contribution to journalArticle

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