Enhanced quantal release of excitatory transmitter in anterior cingulate cortex of adult mice with chronic pain.
Enhanced quantal release of excitatory transmitter in anterior cingulate cortex of adult mice with chronic pain.
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DOI：
10.1186/1744-8069-5-4
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发表时间：
2009-01-27
期刊：
影响因子：
3.3
通讯作者：
Zhuo M
中科院分区：
文献类型：
--
作者：
Toyoda H;Zhao MG;Zhuo M
前扣带皮层（ACC）是前脑结构，在情绪、学习、记忆和持续疼痛中起重要作用。我们之前的研究表明，ACC突触的兴奋性突触传递增强是由外周炎症和神经损伤引起的。然而，关于其突触前机制的信息很少，因为突触传递增强的来源可能包括神经递质在现有释放位点释放的可能性增强和/或可用囊泡数量的增加。本研究旨在对慢性疼痛的前扣带皮层兴奋性突触进行定量分析，以检查这些增加的来源。定量分析显示，外周炎症小鼠模型中，递质释放概率和可用囊泡数量均增加，而神经性疼痛小鼠模型中，仅递质释放概率增加，可用囊泡数量未增加。此外，我们比较了ACC突触的微型兴奋性突触后电位（mEPSCs）与杏仁核和脊髓等其他与疼痛相关的大脑区域的突触后电位（mEPSCs）。有趣的是，ACC突触中mEPSCs的频率和振幅明显低于杏仁核和脊髓。我们的研究提供了强有力的证据，表明慢性炎症性疼痛增加了递质释放的可能性和可用囊泡的数量，而神经性疼痛只增加了ACC突触中递质释放的可能性。
The anterior cingulate cortex (ACC) is a forebrain structure that plays important roles in emotion, learning, memory and persistent pain. Our previous studies have demonstrated that the enhancement of excitatory synaptic transmission was induced by peripheral inflammation and nerve injury in ACC synapses. However, little information is available on their presynaptic mechanisms, since the source of the enhanced synaptic transmission could include the enhanced probability of neurotransmitter release at existing release sites and/or increases in the number of available vesicles. The present study aims to perform quantal analysis of excitatory synapses in the ACC with chronic pain to examine the source of these increases. The quantal analysis revealed that both probability of transmitter release and number of available vesicles were increased in a mouse model of peripheral inflammation, whereas only probability of transmitter release but not number of available vesicles was enhanced in a mouse model of neuropathic pain. In addition, we compared the miniature excitatory postsynaptic potentials (mEPSCs) in ACC synapses with those in other pain-related brain areas such as the amygdala and spinal cord. Interestingly, the rate and amplitude of mEPSCs in ACC synapses were significantly lower than those in the amygdala and spinal cord. Our studies provide strong evidences that chronic inflammatory pain increases both probability of transmitter release and number of available vesicles, whereas neuropathic pain increases only probability of transmitter release in the ACC synapses.
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