在体内重复暴露于可卡因会促进中脑多巴胺神经元中的LTP诱导
Qing-song Liu1, Lu Pu, Mu-ming Poo
1Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA. qsliu@berkeley.edu
Nature
|October 14, 2005
概括
重复暴露于可卡因会通过减少GABA(A) 受体抑制来增强腹膜区域 (VTA) 多巴胺神经元的突触可塑性. 这促进了长期增强 (LTP),可能有助于药物相关的记忆形成.
科学领域:
- 神经科学是一个神经科学.
- 神经药理学神经药理学
- 成研究 研究成研究
背景情况:
- 滥用药物会改变神经回路,导致成.
- 腹膜层区域 (VTA) 多巴胺神经元突触可塑性与药物诱导的电路修改有关.
研究的目的:
- 为了研究重复接触可卡因对大鼠VTA多巴胺神经元突触可塑性的影响.
- 确定GABA (A) 受体介导抑制在可卡因诱导的突触变化中的作用.
主要方法:
- 在老鼠体内重复使用可卡因.
- 中脑切片中的电生理记录,以评估长期强化 (LTP) 诱导.
- 药理学操纵GABA (A) 受体活性,使用比库库林,皮克罗毒素和西帕姆.
主要成果:
- 重复暴露于可卡因促进了激发性突触对VTA多巴胺神经元的LTP诱导.
- 这种促进与可卡因诱导的GABA (A) 受体中介抑制的减少有关.
- 增强的GABAergic抑制阻止了可卡因诱导的LTP,而减少抑制是必要的诱导在幼稚的老鼠.
- 可卡因治疗降低了GABA介导的突触电流幅度,并增加了VTA多巴胺神经元中的尖端启动概率.
结论:
- 重复暴露于可卡因会增加VTA多巴胺神经元中的突触可塑性.
- 减少GABA (A) 受体抑制是这种增强可塑性的关键机制.
- 可卡因诱导的VTA突触可塑性可能在形成与药物相关的记忆中发挥作用.
相关概念视频
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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