Δ9 - 四大麻素自给药诱导细胞类型特异性适应在核的核心
Constanza Garcia-Keller1,2, Madeline Hohmeister1, Kailyn Seidling1
1Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA.
Addiction biology
|July 27, 2023
概括
大麻使用,特别是THC+CBD,会改变D1神经元中的大脑通路,影响谷氨酸的传输和CB1受体的功能. 这些变化可能为治疗大麻使用障碍提供新的目标.
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:
- 滥用药物会导致细胞特异性变化在核核 (NAcore),可能会增加复发风险.
- 在中等脊状神经元 (MSN) 上,Δ9-四大麻 (THC) 的神经适应作用尚不清楚.
研究的目的:
- 调查THC+cannabidiol (CBD) 自给和灭绝是否会在D1-MSN和D2-MSN中诱导细胞类型特定的神经适应.
- 检查THC+CBD对脊柱形态,谷氨酸传播,CB1受体 (CB1R) 功能和神经元活动的影响.
主要方法:
- 使用D1-和D2-Cre转基因大鼠感染了Cre-依赖的记者.
- 训练老鼠自行注射THC+CBD,然后进行灭绝训练.
- 量化了脊柱形态,谷氨酸转移,CB1R功能和灭绝后的cFOS表达.
主要成果:
- THC+CBD的灭绝导致了脊柱头部的丧失和D1-MSN中的谷氨酸转移的减少,同时导致了前突触CB1R功能受损.
- 在D1-MSN中CB1R适应增加了谷氨酸增强能力.
- D2-MSN突触在CB1R功能或谷氨酸传递中没有显著变化,但表现出改变的cFOS表达模式.
结论:
- 使用THC+CBD会诱导D1-MSN中的独特神经适应,影响突触可塑性和神经元活动.
- 在D1-MSN中对内分泌大麻素 (eCB) 信号的特定途径调制为大麻使用障碍 (CUD) 的潜在治疗策略.
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