Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor

Eun Joo Shin; Jong Seok Chae; Myung Eun Jung; Guoying Bing; Kwang Ho Ko; Won Ki Kim; Myung Bok Wie; Mi Ae Cheon; Seung Yeol Nah; Hyoung Chun Kim

doi:10.1016/j.eplepsyres.2006.11.004

Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor

Eun Joo Shin, Jong Seok Chae, Myung Eun Jung, Guoying Bing, Kwang Ho Ko, Won Ki Kim, Myung Bok Wie, Mi Ae Cheon, Seung Yeol Nah, Hyoung Chun Kim

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

Abstract

We examined whether (-)-nicotine infusion can affect kainic acid (KA)-induced neurotoxicity in rats. Although treatment with a single nicotine infusion (0.5 or 1.0 μg/side, i.c.v.) failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 μg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. α-Bungarotoxin and mecamylamine blocked the neuroprotective effects of nicotine. These results suggest that repeated nicotine treatment provides α7 nicotinic acetylcholine receptor-mediated neuroprotection against KA toxicity.

Original language	English
Pages (from-to)	292-298
Number of pages	7
Journal	Epilepsy Research
Volume	73
Issue number	3
DOIs	https://doi.org/10.1016/j.eplepsyres.2006.11.004
Publication status	Published - 2007 Mar
Externally published	Yes

Keywords

AP-1 DNA binding activity
Hippocampus
Kainic acid
Neuroprotection
Nicotine
α7 nicotinic acetylcholine receptor

ASJC Scopus subject areas

Neurology
Clinical Neurology

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Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor. / Shin, Eun Joo; Chae, Jong Seok; Jung, Myung Eun; Bing, Guoying; Ko, Kwang Ho; Kim, Won Ki; Wie, Myung Bok; Cheon, Mi Ae; Nah, Seung Yeol; Kim, Hyoung Chun.

In: Epilepsy Research, Vol. 73, No. 3, 03.2007, p. 292-298.

Research output: Contribution to journal › Article › peer-review

Shin, Eun Joo ; Chae, Jong Seok ; Jung, Myung Eun ; Bing, Guoying ; Ko, Kwang Ho ; Kim, Won Ki ; Wie, Myung Bok ; Cheon, Mi Ae ; Nah, Seung Yeol ; Kim, Hyoung Chun. / Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor. In: Epilepsy Research. 2007 ; Vol. 73, No. 3. pp. 292-298.

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title = "Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor",

abstract = "We examined whether (-)-nicotine infusion can affect kainic acid (KA)-induced neurotoxicity in rats. Although treatment with a single nicotine infusion (0.5 or 1.0 μg/side, i.c.v.) failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 μg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. α-Bungarotoxin and mecamylamine blocked the neuroprotective effects of nicotine. These results suggest that repeated nicotine treatment provides α7 nicotinic acetylcholine receptor-mediated neuroprotection against KA toxicity.",

keywords = "AP-1 DNA binding activity, Hippocampus, Kainic acid, Neuroprotection, Nicotine, α7 nicotinic acetylcholine receptor",

author = "Shin, {Eun Joo} and Chae, {Jong Seok} and Jung, {Myung Eun} and Guoying Bing and Ko, {Kwang Ho} and Kim, {Won Ki} and Wie, {Myung Bok} and Cheon, {Mi Ae} and Nah, {Seung Yeol} and Kim, {Hyoung Chun}",

note = "Funding Information: This research was supported by a Grant (M103KV010013-06K22010310) from the Brain Research Center from 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea, by a Grant of the Korea Health 21 R & D Project (A020007), Ministry of Health & welfare, Republic of Korea, and by BK 21 Project, Korea Research Foundation. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used for this study.",

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doi = "10.1016/j.eplepsyres.2006.11.004",

language = "English",

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AU - Kim, Won Ki

AU - Wie, Myung Bok

AU - Cheon, Mi Ae

AU - Nah, Seung Yeol

AU - Kim, Hyoung Chun

N1 - Funding Information: This research was supported by a Grant (M103KV010013-06K22010310) from the Brain Research Center from 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea, by a Grant of the Korea Health 21 R & D Project (A020007), Ministry of Health & welfare, Republic of Korea, and by BK 21 Project, Korea Research Foundation. Equipment at the Institute of Pharmaceutical Science (Kangwon National University) was used for this study.

PY - 2007/3

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N2 - We examined whether (-)-nicotine infusion can affect kainic acid (KA)-induced neurotoxicity in rats. Although treatment with a single nicotine infusion (0.5 or 1.0 μg/side, i.c.v.) failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 μg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. α-Bungarotoxin and mecamylamine blocked the neuroprotective effects of nicotine. These results suggest that repeated nicotine treatment provides α7 nicotinic acetylcholine receptor-mediated neuroprotection against KA toxicity.

AB - We examined whether (-)-nicotine infusion can affect kainic acid (KA)-induced neurotoxicity in rats. Although treatment with a single nicotine infusion (0.5 or 1.0 μg/side, i.c.v.) failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 μg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. α-Bungarotoxin and mecamylamine blocked the neuroprotective effects of nicotine. These results suggest that repeated nicotine treatment provides α7 nicotinic acetylcholine receptor-mediated neuroprotection against KA toxicity.

KW - AP-1 DNA binding activity

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Repeated intracerebroventricular infusion of nicotine prevents kainate-induced neurotoxicity by activating the α7 nicotinic acetylcholine receptor

Abstract

Keywords

ASJC Scopus subject areas

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