Fino E, Paille V, Deniau J-M, Venance L
Dynamics and Pathophysiology of Neural Networks, INSERM U-667, Collège de France, Université Pierre et Marie Curie, 11 Place Marcelin Berthelot, Paris Cedex 05, France.
Neuroscience. 2009 Jun 2;160(4):744-54. doi: 10.1016/j.neuroscience.2009.03.015. Epub 2009 Mar 19.
Corticostriatal projections constitute the major inputs to basal ganglia, an ensemble of sub-cortical nuclei involved in the learning of cognitive-motor sequences in response to environmental stimuli. Besides striatal output neurons (medium-sized spiny neurons, MSNs) in charge of the detection of cortical activity, three main classes of interneurons (GABAergic, cholinergic and nitric oxide (NO)-synthase interneurons) tightly regulate the corticostriatal information transfer. Despite the crucial role of NO on neuronal signaling and synaptic plasticity, little is known about corticostriatal synaptic transmission and plasticity at the level of striatal neuronal nitric oxide synthase (nNOS) interneurons. Using a corticostriatal rat brain slice preserving the connections between the somatosensory cortex and the striatal cells, we have explored the synaptic transmission between the cerebral cortex and striatal nNOS interneurons and their capability to develop activity-dependent long-term plasticity based on the quasi-coincident cortical and striatal activities (spike-timing dependent plasticity, STDP). We have observed that cortical pyramidal cells activate monosynaptically and very efficiently the striatal nNOS interneurons. In addition, nNOS interneurons are able to develop strong bidirectional long-term plasticity, following STDP protocols. Indeed, the strength of cortically-evoked response at nNOS interneurons varied as a function of time interval between pre- and postsynaptic activations (Deltat=t(post)-t(pre)). For Deltat<0, excitatory post-synaptic currents (EPSCs) were depressed, peaking at a delay of -25 ms. For Deltat>0, EPSCs depressed for 0<Deltat<+30 ms (peaking at +23 ms) and potentiated for +30<Deltat<+65 ms (peaking at +42 ms). The present study reports a direct connection between the striatal nNOS interneurons and the cerebral cortex, and the existence of long-term synaptic plasticity. In addition, this constitutes the first report of an asymmetric bidirectional STDP, with long-term depression (LTD) induced for Deltat<0 and "early" Deltat>0 and long-term potentiation (LTP) induced by "late" Deltat>0.
皮质纹状体投射构成了基底神经节的主要输入，基底神经节是一组皮层下核团，参与对环境刺激做出反应的认知运动序列的学习。除了负责检测皮层活动的纹状体输出神经元（中型多棘神经元，MSNs）外，三类主要的中间神经元（γ-氨基丁酸能、胆碱能和一氧化氮（NO）合酶中间神经元）紧密调节皮质纹状体的信息传递。尽管NO对神经元信号传导和突触可塑性起着关键作用，但关于纹状体神经元型一氧化氮合酶（nNOS）中间神经元水平上的皮质纹状体突触传递和可塑性却知之甚少。利用保留体感皮层和纹状体细胞之间连接的皮质纹状体大鼠脑片，我们探索了大脑皮层与纹状体nNOS中间神经元之间的突触传递，以及它们基于准同时的皮层和纹状体活动（尖峰时间依赖性可塑性，STDP）发展活动依赖性长期可塑性的能力。我们观察到皮层锥体细胞单突触且非常有效地激活纹状体nNOS中间神经元。此外，按照STDP方案，nNOS中间神经元能够发展出强大的双向长期可塑性。实际上，nNOS中间神经元处皮层诱发反应的强度随突触前和突触后激活之间的时间间隔（Δt = t（后）-t（前））而变化。对于Δt < 0，兴奋性突触后电流（EPSCs）受到抑制，在 -25毫秒的延迟时达到峰值。对于Δt > 0，EPSCs在0 < Δt < +30毫秒时受到抑制（在 +23毫秒时达到峰值），在 +30 < Δt < +65毫秒时增强（在 +42毫秒时达到峰值）。本研究报道了纹状体nNOS中间神经元与大脑皮层之间的直接连接以及长期突触可塑性的存在。此外，这是关于不对称双向STDP的首次报道，其中Δt < 0和“早期”Δt > 0时诱导长期抑制（LTD），“晚期”Δt > 0时诱导长期增强（LTP）。
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