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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2002.6
- 수록면
- 158 - 163 (6page)
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Objectives : Several studies indicate that prolonged ethanol exposure enhances N-methyl-D-aspartate(NMDA) receptor-stimulated nitric oxide(NO) formation, which may play an important role in alcohol dependence, withdrawal, and alcohol-associated brain damage Acamprosate(calcium acetylhomotaunne) is a putative anti-craving drug used to maintain abstinence in alcoholics and appears to interact with NMDA receptor, a subclass of glutamate receptors. The present study was designed to investigate the effects of acamprosate on the expression of mitric oxide synthase(NOS) in the rat brain, following chronic ethanol exposure. NOS expression was assessed by histochemical detection of nicotinamide adenine dinucleotide phosphate(NADPH) -diaphorase activity.
Methods : Adult male Spraque-Dawley rats were used. They were randomly assigned to one of three groups; Ethanol with vehicle treated group(1㏄/㎏/i p.), Ethanol with acamprosate treated group (400㎎/㎏/i.p.), and control group without ethanol exposure. They were given 5% ethanol for 8 weeks. The ethanol with acamprosate treated rats were given acamprosate for 4weeks. Histochemistry for NADPH-diaphorase, a marker for neurons containing NOS, was performed.
Results :
1) In the ethanol with vehicle treated group, the number of NADPH-diaphorase-positive cells was significantly increased in the frontal cortex and dentate gyrus compared with control group.
2) In the ethanol with acamprosate treated group, the number of NADPH-diaphorase-positive cells was significantly decreased in the frontal cortex and dentate gyrus compared with ethanol with vehicle treated group.
Conclusion : The present study supports that acamprosate may attenuate ethanol-induced NMDA-mediated processes, such as NO formation and neurotoxicity. This IS in keeping with the concept of acamprosate acting as NMDA receptor antagonist. Furthermore, theses findings suggest that the possible mechanism invoved in the role of nitric oxide in alcohol dependence.
Methods : Adult male Spraque-Dawley rats were used. They were randomly assigned to one of three groups; Ethanol with vehicle treated group(1㏄/㎏/i p.), Ethanol with acamprosate treated group (400㎎/㎏/i.p.), and control group without ethanol exposure. They were given 5% ethanol for 8 weeks. The ethanol with acamprosate treated rats were given acamprosate for 4weeks. Histochemistry for NADPH-diaphorase, a marker for neurons containing NOS, was performed.
Results :
1) In the ethanol with vehicle treated group, the number of NADPH-diaphorase-positive cells was significantly increased in the frontal cortex and dentate gyrus compared with control group.
2) In the ethanol with acamprosate treated group, the number of NADPH-diaphorase-positive cells was significantly decreased in the frontal cortex and dentate gyrus compared with ethanol with vehicle treated group.
Conclusion : The present study supports that acamprosate may attenuate ethanol-induced NMDA-mediated processes, such as NO formation and neurotoxicity. This IS in keeping with the concept of acamprosate acting as NMDA receptor antagonist. Furthermore, theses findings suggest that the possible mechanism invoved in the role of nitric oxide in alcohol dependence.
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