Department of Physiology, Feinberg School of Medicine, Northwestern University Chicago, IL, USA.
Front Syst Neurosci. 2010 Aug 23;4. doi: 10.3389/fnsys.2010.00039. eCollection 2010.
Plasticity is a crucial component of normal brain function and a critical mechanism for recovery from injury. In vitro, associative pairing of presynaptic spiking and stimulus-induced postsynaptic depolarization causes changes in the synaptic efficacy of the presynaptic neuron, when activated by extrinsic stimulation. In vivo, such paradigms can alter the responses of whole groups of neurons to stimulation. Here, we used in vivo spike-triggered stimulation to drive plastic changes in rat forelimb sensorimotor cortex, which we monitored using a statistical measure of functional connectivity inferred from the spiking statistics of the neurons during normal, spontaneous behavior. These induced plastic changes in inferred functional connectivity depended on the latency between trigger spike and stimulation, and appear to reflect a robust reorganization of the network. Such targeted connectivity changes might provide a tool for rerouting the flow of information through a network, with implications for both rehabilitation and brain-machine interface applications.
可塑性是大脑正常功能的关键组成部分，也是从损伤中恢复的关键机制。在体外，通过外源性刺激激活时，突触前放电与刺激诱导的突触后去极化的关联配对会导致突触前神经元的突触效能发生变化。在体内，这种模式可以改变整个神经元群体对刺激的反应。在这里，我们使用体内尖峰触发刺激来驱动大鼠前肢感觉运动皮层的可塑性变化，我们使用来自正常、自发行为期间神经元尖峰统计的功能连接的统计度量来监测这些变化。这些推断的功能连接中的诱导可塑性变化取决于触发尖峰与刺激之间的潜伏期，并且似乎反映了网络的稳健重组。这种有针对性的连接变化可能为通过网络重新路由信息流提供一种工具，这对康复和脑机接口应用都具有重要意义。
