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首页> 外文期刊>Neuron >Elevated BDNF after cocaine withdrawal facilitates LTP in medial prefrontal cortex by suppressing GABA inhibition.
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Elevated BDNF after cocaine withdrawal facilitates LTP in medial prefrontal cortex by suppressing GABA inhibition.

机译：可卡因撤药后BDNF升高通过抑制GABA抑制作用促进前额内侧皮层的LTP。

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摘要

Medial prefrontal cortex (mPFC) is known to be involved in relapse after cocaine withdrawal, but the underlying cellular mechanism remains largely unknown. Here, we report that after terminating repeated cocaine exposure in rats, a gradual increase in the expression of brain-derived neurotrophic factor (BDNF) in the mPFC facilitates activity-induced long-term potentiation (LTP) of excitatory synapses on layer V pyramidal neurons. This enhanced synaptic plasticity could be attributed to BDNF-induced suppression of GABAergic inhibition in the mPFC by reducing the surface expression of GABA(A) receptors. The BDNF effect was mediated by BDNF-TrkB-phosphatase 2A signaling pathway. Downregulating TrkB expression bilaterally in the mPFC reduced the locomotor hypersensitivity to cocaine 8 days after cocaine withdrawal. Thus, elevated BDNF expression after cocaine withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity-induced persistent potentiation that may contribute to cue-induced drug craving and drug-seeking behavior.
机译：已知可卡因撤药后内侧前额叶皮层（mPFC）参与了复发，但基本的细胞机制仍不清楚。在这里，我们报告说，终止大鼠的可卡因重复暴露后，mPFC中脑源性神经营养因子（BDNF）的表达逐渐增加，促进了活性诱导的V层锥体神经元兴奋性突触的长期增强（LTP）。 。这种增强的突触可塑性可归因于BDNF诱导的mPFC中GABA能抑制的抑制，其通过减少GABA（A）受体的表面表达来实现。 BDNF的作用是由BDNF-TrkB-磷酸酶2A信号通路介导的。可卡因戒断8天后，mPFC中双侧下调TrkB表达降低了对可卡因的运动超敏性。因此，可卡因撤药后BDNF表达的升高使mPFC中的兴奋性突触敏感，使其经历活动诱导的持续增强，这可能有助于线索诱导的药物渴望和药物寻求行为。

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