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논문 기본 정보

자료유형
학술저널
저자정보
Hee Jin Kim (삼육대학교) So Hyun Joo (건국대학교) Inha Choi (건국대학교) Pitna Kim (건국대학교) Min Kyoung Kim (건국대학교) Seung Hwa Park (건국대학교) Jae Hoon Cheong (삼육대학교) Chan Young Shin (건국대학교)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.34 No.1
발행연도
2010.3
수록면
8 - 16 (9page)

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초록· 키워드

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Attention deficit hyperactivity disorder (ADHD) affects 4-12% of chool-age children worldwide and is characterized by three core symptoms: hyperactivity, inattention, and impulsivity. Although standard pharmacological treatments, such as methylphenidate and atomoxetine, are available, concerns about drug-induced psychological and cardiovascular problems, as well as growth retardation and sleep disturbances, highlight the continuing need for new therapeutic interventions. Using a neonatal hypoxia-induced hyperactivity model in rats, the potential positive role that oral administration of red ginseng extract may have in relation to the hyperactive phenotype was investigated. Hypoxia was induced in 2-day-old male Sprague-Dawley (SD) rat pups by placing them in a nitrogen chamber for 15 min. The neonatal hypoxia-induced rats showed a significant increase in hyperactivity phenotype, such as increased movement duration, movement distance, and rearing frequency, which was determined by monitoring their spontaneous locomotor activity using the Ethovision video tracking system. One week of oral treatment with red ginseng extract decreased the hyperactivity phenotype of the neonatal hypoxia-induced rats and increased the locomotor activity of the control rats. In the neonatal hypoxia-induced rats, expression of the norepinephrine transporter in the forebrain was increased, and red ginseng treatment partially prevented its up-regulation, while increasing its level in the control rats. Taken together, these results suggest that red ginseng extract decreased the neonatal hypoxia-induced hyperactivity phenotype, although it increased locomotor activity in normal animals.

목차

Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENT
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2010-524-003375739