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^*

^*Corresponding author for this work

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

Bibliographical 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.

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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10.1016/j.eplepsyres.2006.11.004

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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.",

year = "2007",

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

language = "English",

volume = "73",

pages = "292--298",

journal = "Epilepsy Research",

issn = "0920-1211",

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AU - Shin, Eun Joo

AU - Chae, Jong Seok

AU - Jung, Myung Eun

AU - Bing, Guoying

AU - Ko, Kwang Ho

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

Y1 - 2007/3

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

KW - Hippocampus

KW - Kainic acid

KW - Neuroprotection

KW - Nicotine

KW - α7 nicotinic acetylcholine receptor

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DO - 10.1016/j.eplepsyres.2006.11.004

M3 - Article

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AN - SCOPUS:33847189602

SN - 0920-1211

VL - 73

SP - 292

EP - 298

JO - Epilepsy Research

JF - Epilepsy Research

IS - 3

ER -

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

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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