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

Neuroscience

Producción científica: Article › revisión exhaustiva

17 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	292-298
Número de páginas	7
Publicación	Epilepsy Research
Volumen	73
N.º	3
DOI	https://doi.org/10.1016/j.eplepsyres.2006.11.004
Estado	Published - mar 2007

Nota bibliográfica

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.

Financiación

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.

Financiadores	Número del financiador
BK 21 Project
Korean Ministry of Health and Welfare
Department of Science and Technology, Ministry of Science and Technology, India	A020007
Department of Science and Technology, Ministry of Science and Technology, India
National Research Foundation of Korea

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.",

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language = "English",

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AU - Chae, Jong Seok

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AU - Bing, Guoying

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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

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.

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KW - Kainic acid

KW - Neuroprotection

KW - Nicotine

KW - α7 nicotinic acetylcholine receptor

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

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ASJC Scopus subject areas

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