Ginsenosides attenuate methamphetamine-induced behavioral side effects in mice via activation of adenosine A2A receptors

Possible involvements of the striatal reduction in AP-1 DNA binding activity and proenkephalin gene expression

Eun Joo Shin, Toshitaka Nabeshima, Hong Won Suh, Wang Kee Jhoo, Ki Wan Oh, Yong Kwang Lim, Dong Sup Kim, Ki Hwan Choi, Hyoung Chun Kim

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Current evidence suggests that ginsenosides inhibit methamphetamine (MA)-induced changes in behavior, but the precise mechanisms that underlie this effect are yet to be determined. We examined the role of adenosine receptors in the ginsenoside-induced changes in hyperlocomotion and conditioned place preference (CPP) in mice that occurred in response to administration of MA (2 mg/kg, i.p. × 1 or 2 mg/kg, i.p. × 6). Changes in circling behavior paralleled changes in CPP in the presence of MA. Pre-treatment with ginsenosides (50 or 150 mg/kg, i.p.) attenuated the MA-induced circling behavior and CPP. This attenuation was reversed by the adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chrostyryl)xanthine (CSC; 0.5 and 1.0 mg/kg) in a dose-dependent manner, but neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 0.5 and 1.0 mg/kg) nor the A2B receptor antagonist alloxazine (ALX; 1.5 and 3.0 mg/kg) had any such effect. MA-induced increases in activator protein (AP)-1 DNA binding activity, Fos-related antigen immunoreactivity (FRA-IR), proenkephalin mRNA expression, and proenkephalin-like immunoreactivity were reduced consistently in the striatum of animals that were pretreated with ginsenosides. These reductions were largely prevented by CSC, but not by CPT or ALX. Our results suggest that the stimulation of A2A receptors by ginsenosides attenuates the changes in behavior and the increases in AP-1 DNA binding activity, FRA-IR, and proenkephalin gene expression in mouse striatum that are induced by MA.

Original languageEnglish
Pages (from-to)143-157
Number of pages15
JournalBehavioural Brain Research
Volume158
Issue number1
DOIs
Publication statusPublished - 07-03-2005

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Adenosine A2A Receptors
Ginsenosides
Corpus Striatum
Methamphetamine
Transcription Factor AP-1
Gene Expression
DNA
Proto-Oncogene Proteins c-fos
Adenosine A2 Receptor Antagonists
Adenosine A1 Receptor Antagonists
Purinergic P1 Receptors
Xanthine
proenkephalin
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Behavioral Neuroscience

Cite this

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title = "Ginsenosides attenuate methamphetamine-induced behavioral side effects in mice via activation of adenosine A2A receptors: Possible involvements of the striatal reduction in AP-1 DNA binding activity and proenkephalin gene expression",
abstract = "Current evidence suggests that ginsenosides inhibit methamphetamine (MA)-induced changes in behavior, but the precise mechanisms that underlie this effect are yet to be determined. We examined the role of adenosine receptors in the ginsenoside-induced changes in hyperlocomotion and conditioned place preference (CPP) in mice that occurred in response to administration of MA (2 mg/kg, i.p. × 1 or 2 mg/kg, i.p. × 6). Changes in circling behavior paralleled changes in CPP in the presence of MA. Pre-treatment with ginsenosides (50 or 150 mg/kg, i.p.) attenuated the MA-induced circling behavior and CPP. This attenuation was reversed by the adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chrostyryl)xanthine (CSC; 0.5 and 1.0 mg/kg) in a dose-dependent manner, but neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 0.5 and 1.0 mg/kg) nor the A2B receptor antagonist alloxazine (ALX; 1.5 and 3.0 mg/kg) had any such effect. MA-induced increases in activator protein (AP)-1 DNA binding activity, Fos-related antigen immunoreactivity (FRA-IR), proenkephalin mRNA expression, and proenkephalin-like immunoreactivity were reduced consistently in the striatum of animals that were pretreated with ginsenosides. These reductions were largely prevented by CSC, but not by CPT or ALX. Our results suggest that the stimulation of A2A receptors by ginsenosides attenuates the changes in behavior and the increases in AP-1 DNA binding activity, FRA-IR, and proenkephalin gene expression in mouse striatum that are induced by MA.",
author = "Shin, {Eun Joo} and Toshitaka Nabeshima and Suh, {Hong Won} and Jhoo, {Wang Kee} and Oh, {Ki Wan} and Lim, {Yong Kwang} and Kim, {Dong Sup} and Choi, {Ki Hwan} and Kim, {Hyoung Chun}",
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Ginsenosides attenuate methamphetamine-induced behavioral side effects in mice via activation of adenosine A2A receptors : Possible involvements of the striatal reduction in AP-1 DNA binding activity and proenkephalin gene expression. / Shin, Eun Joo; Nabeshima, Toshitaka; Suh, Hong Won; Jhoo, Wang Kee; Oh, Ki Wan; Lim, Yong Kwang; Kim, Dong Sup; Choi, Ki Hwan; Kim, Hyoung Chun.

In: Behavioural Brain Research, Vol. 158, No. 1, 07.03.2005, p. 143-157.

Research output: Contribution to journalArticle

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T2 - Possible involvements of the striatal reduction in AP-1 DNA binding activity and proenkephalin gene expression

AU - Shin, Eun Joo

AU - Nabeshima, Toshitaka

AU - Suh, Hong Won

AU - Jhoo, Wang Kee

AU - Oh, Ki Wan

AU - Lim, Yong Kwang

AU - Kim, Dong Sup

AU - Choi, Ki Hwan

AU - Kim, Hyoung Chun

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N2 - Current evidence suggests that ginsenosides inhibit methamphetamine (MA)-induced changes in behavior, but the precise mechanisms that underlie this effect are yet to be determined. We examined the role of adenosine receptors in the ginsenoside-induced changes in hyperlocomotion and conditioned place preference (CPP) in mice that occurred in response to administration of MA (2 mg/kg, i.p. × 1 or 2 mg/kg, i.p. × 6). Changes in circling behavior paralleled changes in CPP in the presence of MA. Pre-treatment with ginsenosides (50 or 150 mg/kg, i.p.) attenuated the MA-induced circling behavior and CPP. This attenuation was reversed by the adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chrostyryl)xanthine (CSC; 0.5 and 1.0 mg/kg) in a dose-dependent manner, but neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 0.5 and 1.0 mg/kg) nor the A2B receptor antagonist alloxazine (ALX; 1.5 and 3.0 mg/kg) had any such effect. MA-induced increases in activator protein (AP)-1 DNA binding activity, Fos-related antigen immunoreactivity (FRA-IR), proenkephalin mRNA expression, and proenkephalin-like immunoreactivity were reduced consistently in the striatum of animals that were pretreated with ginsenosides. These reductions were largely prevented by CSC, but not by CPT or ALX. Our results suggest that the stimulation of A2A receptors by ginsenosides attenuates the changes in behavior and the increases in AP-1 DNA binding activity, FRA-IR, and proenkephalin gene expression in mouse striatum that are induced by MA.

AB - Current evidence suggests that ginsenosides inhibit methamphetamine (MA)-induced changes in behavior, but the precise mechanisms that underlie this effect are yet to be determined. We examined the role of adenosine receptors in the ginsenoside-induced changes in hyperlocomotion and conditioned place preference (CPP) in mice that occurred in response to administration of MA (2 mg/kg, i.p. × 1 or 2 mg/kg, i.p. × 6). Changes in circling behavior paralleled changes in CPP in the presence of MA. Pre-treatment with ginsenosides (50 or 150 mg/kg, i.p.) attenuated the MA-induced circling behavior and CPP. This attenuation was reversed by the adenosine A2A receptor antagonist 1,3,7-trimethyl-8-(3-chrostyryl)xanthine (CSC; 0.5 and 1.0 mg/kg) in a dose-dependent manner, but neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 0.5 and 1.0 mg/kg) nor the A2B receptor antagonist alloxazine (ALX; 1.5 and 3.0 mg/kg) had any such effect. MA-induced increases in activator protein (AP)-1 DNA binding activity, Fos-related antigen immunoreactivity (FRA-IR), proenkephalin mRNA expression, and proenkephalin-like immunoreactivity were reduced consistently in the striatum of animals that were pretreated with ginsenosides. These reductions were largely prevented by CSC, but not by CPT or ALX. Our results suggest that the stimulation of A2A receptors by ginsenosides attenuates the changes in behavior and the increases in AP-1 DNA binding activity, FRA-IR, and proenkephalin gene expression in mouse striatum that are induced by MA.

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