Walters E T, Cohen L B
Department of Integrative Biology and Pharmacology, University of Texas-Houston Medical School 77030, USA.
Invert Neurosci. 1997 Jun;3(1):15-25. doi: 10.1007/BF02481711.
Mechanosensory neurons which innervate the siphon and have their cell bodies in the LE cluster of the abdominal ganglion of Aplysia have revealed many cellular and molecular processes that may play general roles in learning and memory. It was initially suggested that these cells are largely responsible for triggering the gill-withdrawal reflex evoked by weak siphon stimulation, and that most of this effect is mediated by their monosynaptic connections to gill motor neurons. This implied a simple link between plasticity at these synapses and modifications of the reflex during learning. We review more recent studies from several laboratories showing that the LE cells are not activated by very weak tactile stimuli that elicit the gill-withdrawal reflex, and that an unidentified population of siphon sensory neurons has lower mechanosensory thresholds and produces shorter latency responses. Furthermore, the direct connections between LE cells and gill motor neurons make a minor contribution when the reflex is elicited in pinned siphon preparations by light stimuli that weakly activate the LE cells. Because weak mechanical stimulation of the unrestrained siphon causes little or no LE cell activation, it is unlikely that, under natural conditions, sensitization or conditioning of reflex responses elicited by light siphon touch depends upon plasticity of LE cell synapses onto either motor or interneurons. The LE cells appear to function as nociceptors because they are tuned to noxious stimuli and, like mammalian nociceptors, show peripheral sensitization following nociceptive activation. This sensitization and the profound activity-dependent potentiation of LE synapses indicate that LE cell contributions to defensive reflexes should be largest during and after intense activation of the LE cells by noxious stimulation (with the LE cell plasticity contributing to long-lasting memory of peripheral injury). The LE sensory neurons offer special opportunities for direct tests of this and other hypotheses about specific mnemonic functions of fundamental mechanisms of neural plasticity.
支配虹吸管且细胞体位于海兔腹神经节LE簇的机械感觉神经元，已揭示出许多可能在学习和记忆中发挥普遍作用的细胞和分子过程。最初有人提出，这些细胞在很大程度上负责触发由弱虹吸管刺激诱发的鳃收缩反射，并且这种效应的大部分是由它们与鳃运动神经元的单突触连接介导的。这意味着这些突触的可塑性与学习过程中反射的改变之间存在简单的联系。我们回顾了几个实验室最近的研究，这些研究表明，LE细胞不会被引发鳃收缩反射的非常弱的触觉刺激激活，并且一群身份不明的虹吸管感觉神经元具有较低的机械感觉阈值并产生潜伏期更短的反应。此外，当在固定虹吸管标本中通过弱激活LE细胞的光刺激诱发反射时，LE细胞与鳃运动神经元之间的直接连接所起的作用较小。由于对无束缚虹吸管的弱机械刺激几乎不会或根本不会激活LE细胞，因此在自然条件下，由光虹吸管触摸诱发的反射反应的敏感化或条件作用不太可能依赖于LE细胞与运动神经元或中间神经元突触的可塑性。LE细胞似乎起着伤害感受器的作用，因为它们对有害刺激有反应，并且像哺乳动物的伤害感受器一样，在伤害性激活后会出现外周敏化。这种敏化以及LE突触的深度活动依赖性增强表明，在LE细胞被有害刺激强烈激活期间和之后，LE细胞对防御反射的贡献应该最大（LE细胞的可塑性有助于对外周损伤的长期记忆）。LE感觉神经元为直接测试关于神经可塑性基本机制的特定记忆功能的这一假设和其他假设提供了特殊机会。
