Stanson Toshok Center for Brain Function and Repair, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, United States.
Department of Cell Biology and Anatomy, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, United States.
J Neurophysiol. 2024 Jul 1;132(1):96-107. doi: 10.1152/jn.00001.2024. Epub 2024 May 22.
In response to a suitably aversive skin stimulus, the marine mollusk launches an escape swim followed by several minutes of high-speed crawling. The two escape behaviors are highly dissimilar: whereas the swim is a muscular behavior involving alternating ventral and dorsal whole body flexions, the crawl is a nonrhythmic gliding behavior mediated by the beating of foot cilia. The serotonergic dorsal swim interneurons (DSIs) are members of the swim central pattern generator (CPG) and also strongly drive crawling. Although the swim network is very well understood, the crawling network to date comprises only three neurons: the DSIs and pedal neurons 5 and 21 (Pd5 and Pd21). Since s swim network has been suggested to have arisen from a preexisting crawling network, we examined the possible role that another swim CPG neuron, C2, may play in crawling. Because of its complete silence in the postswim crawling period, C2 had not previously been considered to play a role in driving crawling. However, semi-intact preparation experiments demonstrated that a brief C2 spike train surprisingly and strongly drives the foot cilia for ∼30 s, something that cannot be explained by its synaptic connections to Pd5 and Pd21. Voltage-sensitive dye (VSD) imaging in the pedal ganglion identified many candidate crawling motor neurons that fire at an elevated rate after the swim and also revealed several pedal neurons that are strongly excited by C2. It is intriguing that unlike the DSIs, which fire tonically after the swim to drive crawling, C2 does so despite its postswim silence. swim central pattern generator (CPG) neuron C2 surprisingly and strongly drives the early phase of postswim crawling despite being silent during this period. In decades of research, C2 had not been suspected of driving crawling because of its complete silence after the swim. Voltage-sensitive dye imaging revealed that the crawling motor network may be much larger than previously known and also revealed that many candidate crawling neurons are excited by C2.
对适当的厌恶皮肤刺激做出反应后，海洋软体动物会发起逃避游泳，随后进行几分钟的高速爬行。这两种逃避行为非常不同：游泳是一种肌肉行为，涉及交替的腹侧和背侧全身弯曲，而爬行是一种非节奏性的滑行行为，由足部纤毛的拍打介导。血清素能的背侧游泳中间神经元（DSIs）是游泳中枢模式发生器（CPG）的成员，也强烈驱动爬行。虽然游泳网络已经得到很好的理解，但迄今为止，爬行网络仅包括三个神经元：DSIs 和足神经节 5 和 21 神经元（Pd5 和 Pd21）。由于游泳网络被认为是从先前存在的爬行网络中产生的，因此我们研究了另一个游泳 CPG 神经元 C2 可能在爬行中发挥的作用。由于它在游泳后的爬行期完全沉默，因此 C2 以前并未被认为在驱动爬行中发挥作用。然而，半完整的准备实验表明，C2 的短暂尖峰活动会令人惊讶且强烈地驱动足部纤毛运动约 30 秒，这不能用其与 Pd5 和 Pd21 的突触连接来解释。在足神经节中的电压敏感染料（VSD）成像中，鉴定出许多候选爬行运动神经元，它们在游泳后以升高的频率发射，并且还发现几个足神经元被 C2 强烈兴奋。有趣的是，与游泳后持续驱动爬行的 DSIs 不同，C2 尽管在游泳后保持沉默，但仍会这样做。游泳中枢模式发生器（CPG）神经元 C2 尽管在游泳后保持沉默，但仍令人惊讶且强烈地驱动游泳后的早期爬行阶段。在几十年的研究中，由于 C2 在游泳后完全沉默，因此它一直没有被怀疑用于驱动爬行。电压敏感染料成像显示，爬行运动网络可能比以前已知的要大得多，并且还显示许多候选爬行神经元被 C2 兴奋。
