Svensson Erik, Evans Colin G, Cropper Elizabeth C
Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York.
Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York
J Neurophysiol. 2016 Mar;115(3):1637-43. doi: 10.1152/jn.01082.2015. Epub 2016 Jan 13.
When a behavior is repeated performance often improves, i.e., repetition priming occurs. Although repetition priming is ubiquitous, mediating mechanisms are poorly understood. We address this issue in the feeding network ofAplysia Similar to the priming observed elsewhere, priming inAplysiais stimulus specific, i.e., it can be either "ingestive" or "egestive." Previous studies demonstrated that priming alters motor and premotor activity. Here we sought to determine whether sensorimotor transmission is also modified. We report that changes in sensorimotor transmission do occur. We ask how they are mediated and obtain data that strongly suggest a presynaptic mechanism that involves changes in the "background" intracellular Ca(2+)concentration ([Ca(2+)]i) in primary afferents themselves. This form of plasticity has previously been described and generated interest due to its potentially graded nature. Manipulations that alter the magnitude of the [Ca(2+)]iimpact the efficacy of synaptic transmission. It is, however, unclear how graded control is exerted under physiologically relevant conditions. In the feeding system changes in the background [Ca(2+)]iare mediated by the induction of a nifedipine-sensitive current. We demonstrate that the extent to which this current is induced is altered by peptides (i.e., increased by a peptide released during the repetition priming of ingestive activity and decreased by a peptide released during the repetition priming of egestive activity). We suggest that this constitutes a behaviorally relevant mechanism for the graded control of synaptic transmission via the regulation of the [Ca(2+)]iin a neuron.
当一种行为被重复执行时,其表现通常会得到改善,即出现重复启动效应。尽管重复启动效应普遍存在,但其介导机制却知之甚少。我们在海兔的摄食网络中研究了这个问题。与在其他地方观察到的启动效应类似,海兔中的启动效应具有刺激特异性,也就是说,它可以是“摄食性的”或“排粪性的”。先前的研究表明,启动效应会改变运动和运动前的活动。在这里,我们试图确定感觉运动传递是否也会被改变。我们报告感觉运动传递确实发生了变化。我们探究这些变化是如何介导的,并获得了有力的数据,表明这是一种突触前机制,涉及初级传入神经元自身“背景”细胞内钙离子浓度([Ca(2+)]i)的变化。这种可塑性形式此前已有描述,并因其潜在的分级性质而引起了人们的兴趣。改变[Ca(2+)]i大小的操作会影响突触传递的效能。然而,目前尚不清楚在生理相关条件下如何实现分级控制。在摄食系统中,背景[Ca(2+)]i的变化是由硝苯地平敏感电流的诱导介导的。我们证明,这种电流的诱导程度会受到肽的影响(即,在摄食活动的重复启动过程中释放的一种肽会使其增加,而在排粪活动的重复启动过程中释放的一种肽会使其减少)。我们认为,这构成了一种通过调节神经元内[Ca(2+)]i对突触传递进行分级控制的行为相关机制。