デキスフェンフルーラミンの神経毒性は,人間以外の霊長類の脳にみられる
G A Ricaurte1, M E Molliver, M B Martello
1Department of Neurology, Francis Scott Key Medical Center, Johns Hopkins School of Medicine, Baltimore, Maryland 21224.
Lancet (London, England)
|December 14, 1991
まとめ
食欲抑制剤であるデックスフェンフルラミンは,サルにおける脳セロトニン (5-HT) ニューロンを損傷することが判明しました. この神経毒性は,ヒトにおける薬物の安全性について懸念を喚起しています.
科学分野:
- 神経科学は神経科学である.
- 薬理学 薬理学とは
- 毒理学 毒理学 毒理学
背景:
- デックスフェンフルラミンは食欲抑制剤です.
- セロトニン (5-HT) ニューロンは,様々な脳の機能に不可欠です.
- デキスフェンフルラミンの潜在的な神経毒性作用は,調査を必要とする.
研究 の 目的:
- 非ヒト霊長類におけるセロトニン (5-HT) ニューロンに対するデクスフェンフルラミンの神経毒性可能性を評価する.
主な方法:
- リス類は,デキスフェンフルラミンを4日間,毎日2回,皮膚下に投与した.
- 投与された用量は1.25 mg/kgまたは5.00 mg/kgであった.
- 神経化学的および形態学的評価は,治療後2週間で行われました.
主要な成果:
- セロトニン (5-HT) と5ヒドロキシインデレアセティック酸の投与量による減少が観察されました.
- 5-HT吸収部位の減少が検出されました.
- 形態学的研究では,急性軸突の変化と5-HT軸突密度の持続的な減少が示されました.
結論:
- デックスフェンフルラミンは,サルにおけるセロトニン (5-HT) 中枢神経細胞に損傷を与える.
- この発見は,人間におけるデクスフェンフルラミンの潜在的な神経毒性を示唆しています.
- 長期的な影響を理解するためにさらなる研究が必要である.
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