在AMPA受体中因灭绝引起的上调减少了寻找可卡因的行为
Michael A Sutton1, Eric F Schmidt, Kwang-Ho Choi
1Division of Molecular Psychiatry and the Interdepartmental Neuroscience Program, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
Nature
|January 4, 2003
概括
对于可卡因成的灭绝训练会增加大脑中的AMPA谷氨酸酸受体. 这种神经可塑性有助于减少可卡因寻找和复发,即使在压力下.
科学领域:
- 神经科学是一个神经科学.
- 神经生物学 神经生物学 神经生物学
- 成研究 研究成研究
背景情况:
- 可卡因成涉及持续的神经生物学变化,导致复发.
- 灭绝训练是一种抑制性学习形式,可以通过将药物线索与没有奖励联系起来来减少寻找可卡因的行为.
研究的目的:
- 为了研究在减少可卡因寻求的灭绝训练的有效性背后的神经生物学机制.
- 在灭绝学习过程中确定AMPA谷氨酸受体在核突外中的作用.
主要方法:
- 慢性可卡因自我管理,随后在动物模型中进行戒断和灭绝培训.
- 测量AMPA受体子单元表达 (GluR1,GluR2/3) 在核内外.
- 病毒介导的GluR1和GluR2在核突中的过度基因表达.
主要成果:
- 灭绝训练增加了核突贝中的GluR1和GluR2/3 AMPA受体子单元.
- 增加的GluR1表达与实现的灭绝程度正相关.
- 过度表达GluR1和GluR2有助于可卡因寻找的物种灭绝,但没有使得寻求糖的物种灭绝.
- 在过度表达期间单次灭绝会话减轻了压力诱导的复发.
结论:
- 在核突贝中的AMPA受体中,灭绝诱导的可塑性促进了对可卡因寻找的控制.
- 这种可塑性可能会恢复谷氨酸质基调,并降低禁欲个体的复发倾向,特别是在压力下.
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