Cholinergic interneurons control the excitatory input to the striatum
Cholinergic interneurons control the excitatory input to the striatum
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DOI：
10.1523/jneurosci.3709-06.2007
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发表时间：
2007-01-10
影响因子：
5.3
通讯作者：
Bracci, Enrico
中科院分区：
文献类型：
--
作者：
Pakhotin, Pavel;Bracci, Enrico
突触前抑制的程度和时间过程如何取决于控制末梢的神经元的动作电位尚不清楚。我们研究了这个问题，在纹状体使用配对记录胆碱能中间神经元和投射神经元。谷氨酸能EPSC诱发的投射神经元和胆碱能中间神经元的皮层和纹状体的传入纤维的刺激，分别。胆碱能中间神经元中的单个尖峰引起34%的投射神经元位于100 μ m内和41%的胆碱能中间神经元位于200 μ m内的诱发的神经元兴奋性EPSC的显著抑郁。在这两种情况下，这些影响的时间过程是相似的，与EPSC抑制峰值后20-30毫秒的尖峰和消失后40-80毫秒。EPSC振幅的最大抑郁症是高达27%的投射神经元和胆碱能中间神经元的19%。这些作用可逆地阻断毒蕈碱受体拮抗剂（阿托品或甲氧四明），这也显着增加基线EPSC（诱发没有在胆碱能中间神经元的前穗），表明一些紧张性胆碱能突触前抑制。这一点得到了以下事实的证实：降低细胞外钾，沉默自发活性胆碱能中间神经元，也增加了基线EPSC振幅，这些作用被先前应用的毒蕈碱受体拮抗剂所阻断。总的来说，这些结果表明，一个单一的尖峰胆碱能中间神经元施加一个快速和强大的抑制性控制纹状体神经元的多巴胺能输入。
How the extent and time course of presynaptic inhibition depend on the action potentials of the neuron controlling the terminals is unknown. We investigated this issue in the striatum using paired recordings from cholinergic interneurons and projection neurons. Glutamatergic EPSCs were evoked in projection neurons and cholinergic interneurons by stimulation of afferent fibers in the cortex and the striatum, respectively. A single spike in a cholinergic interneuron caused significant depression of the evoked glutamatergic EPSC in 34% of projection neurons located within 100 mu m and 41% of cholinergic interneurons located within 200 mu m. The time course of these effects was similar in the two cases, with EPSC inhibition peaking 20-30 ms after the spike and disappearing after 40-80 ms. Maximal depression of EPSC amplitude was up to 27% in projection neurons and to 19% in cholinergic interneurons. These effects were reversibly blocked by muscarinic receptor antagonists (atropine or methoctramine), which also significantly increased baseline EPSC (evoked without a preceding spike in the cholinergic interneuron), suggesting that some tonic cholinergic presynaptic inhibition was present. This was confirmed by the fact that lowering extracellular potassium, which silenced spontaneously active cholinergic interneurons, also increased baseline EPSC amplitude, and these effects were occluded by previous application of muscarinic receptor antagonists. Collectively, these results show that a single spike in a cholinergic interneuron exerts a fast and powerful inhibitory control over the glutamatergic input to striatal neurons.