Feedforward compensation mediated by the central and peripheral actions of a single neuropeptide discovered using representational difference analysis.
Feedforward compensation mediated by the central and peripheral actions of a single neuropeptide discovered using representational difference analysis.
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DOI：
10.1523/jneurosci.4264-10.2010
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发表时间：
2010-12-08
期刊：
影响因子：
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通讯作者：
Vilim FS
中科院分区：
文献类型：
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作者：
Jing J;Sweedler JV;Cropper EC;Alexeeva V;Park JH;Romanova EV;Xie F;Dembrow NC;Ludwar BC;Weiss KR;Vilim FS
补偿机制通常用于通过减少方差来实现稳定性，这可以通过在稳态调节期间的负反馈来实现。原则上，补偿也可以通过前馈机制来实现，其中调节器的作用是抵消预期的输出变化；然而，这种神经机制很少被证实。我们提供的证据表明，一种应用增强的代表性差异分析程序识别的海雀神经肽，在进食网络中实现了前馈补偿。由于其与昆虫的allatotropin相似，我们将其命名为allatotropin-related peptide （ATRP）。质谱分析证实了该肽的身份，原位杂交和免疫染色确定了其在大头蛇中枢神经系统中的分布。ATRP存在于高阶脑颊间神经元（CBI）， CBI-4，但不存在于CBI-2。先前的研究表明，cbi -4诱发的运动项目比CBI-2诱发的运动项目具有更短的持续时间。本研究表明，ATRP缩短了cbi -2诱导的摄取程序的延长时间，表明ATRP对CBI-4和cbi -2诱发的程序之间的参数差异有贡献。重要的是，由于伸肌收缩是运动神经元活动的分级功能，伸肌缩短的一个后果是它会削弱伸肌运动。然而，这种潜在的减弱被ATRP施加的前馈补偿作用所抵消。在中枢，ATRP增加拉伸运动神经元的活性。此外，ATRP存在于外周拉伸运动神经元的静脉曲张中，并增强外周运动神经元引起的拉伸肌肉收缩。因此，由ATRP介导的前馈补偿机制可以产生更快的运动，且振幅不会大大降低，从而产生稳定性。
Compensatory mechanisms are often used to achieve stability by reducing variance, which can be accomplished via negative feedback during homeostatic regulation. In principle, compensation can also be implemented through feedforward mechanisms where a regulator acts to offset the anticipated output variation; however, few such neural mechanisms have been demonstrated. We provide evidence that an Aplysia neuropeptide, identified using an enhanced representational difference analysis procedure, implements feedforward compensation within the feeding network. We named the novel peptide allatotropin-related peptide (ATRP) because of its similarity to insect allatotropin. Mass spectrometry confirmed the peptide's identity, and in situ hybridization and immunostaining mapped its distribution in the Aplysia CNS. ATRP is present in the higher-order cerebral-buccal interneuron (CBI), CBI-4, but not in CBI-2. Previous work showed that CBI-4-elicited motor programs have a shorter protraction duration than those elicited by CBI-2. Here we show that ATRP shortens protraction duration of CBI-2-elicited ingestive programs, suggesting a contribution of ATRP to the parametric differences between CBI-4- and CBI-2-evoked programs. Importantly, because Aplysia muscle contractions are a graded function of motoneuronal activity, one consequence of the shortening of protraction is that it can weaken protraction movements. However, this potential weakening is offset by feedforward compensatory actions exerted by ATRP. Centrally, ATRP increases the activity of protraction motoneurons. Moreover, ATRP is present in peripheral varicosities of protraction motoneurons and enhances peripheral motoneuron-elicited protraction muscle contractions. Therefore, feedforward compensatory mechanisms mediated by ATRP make it possible to generate a faster movement with an amplitude that is not greatly reduced, thereby producing stability.