Role of nitric oxide in classical conditioning of siphon withdrawal in Aplysia
Role of nitric oxide in classical conditioning of siphon withdrawal in Aplysia
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DOI：
10.1523/jneurosci.2357-07.2007
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发表时间：
2007-10-10
影响因子：
5.3
通讯作者：
Hawkins, Robert D.
中科院分区：
文献类型：
--
作者：
Antonov, Igor;Ha, Thomas;Hawkins, Robert D.
一氧化氮 (NO) 被认为参与多种形式的体内学习和体外突触可塑性，但人们对一氧化氮在学习过程中发生的可塑性生理形式中的作用知之甚少。我们通过简化海兔虹吸回缩反射的准备来解决这个问题。我们首先使用原位杂交来证明所鉴定的 L29 促进神经元表达 NO 合酶。此外，外源性 NO 会促进感觉运动神经元 EPSP，而 NO 合酶抑制剂或 NO 清除剂会阻碍行为调节。将清除剂应用于神经节或注射到感觉神经元中会阻断 EPSP 的促进以及调节过程中感觉神经元膜特性的变化。将清除剂注射到运动神经元中会降低促进作用，但不会影响感觉神经元膜的特性，而注射一氧化氮合酶抑制剂则没有效果。突触后注射胞吐作用抑制剂具有与注射清除剂类似的效果。然而，调节过程中 EPSP 形状的变化与突触后 AMPA 样受体插入不一致，而是被突触前尖峰加宽所模仿。这些结果表明，NO 在调节过程中发挥着重要作用，并直接作用于感觉神经元和运动神经元，影响它们之间突触的不同促进过程。此外，他们认为 NO 既不是来自感觉神经元，也不是来自运动神经元，而是来自另一个来源，可能是 L29 中间神经元。
Nitric oxide ( NO) is thought to be involved in several forms of learning in vivo and synaptic plasticity in vitro, but very little is known about the role of NO during physiological forms of plasticity that occur during learning. We addressed that question in a simplified preparation of the Aplysia siphon-withdrawal reflex. We first used in situ hybridization to show that the identified L29 facilitator neurons express NO synthase. Furthermore, exogenous NO produced facilitation of sensory-motor neuron EPSPs, and an inhibitor of NO synthase or an NO scavenger blocked behavioral conditioning. Application of the scavenger to the ganglion or injection into a sensory neuron blocked facilitation of the EPSP and changes in the sensory-neuron membrane properties during conditioning. Injection of the scavenger into the motor neuron reduced facilitation without affecting sensory neuron membrane properties, and injection of an inhibitor of NO synthase had no effect. Postsynaptic injection of an inhibitor of exocytosis had effects similar to injection of the scavenger. However, changes in the shape of the EPSP during conditioning were not consistent with postsynaptic AMPA-like receptor insertion but were mimicked by presynaptic spike broadening. These results suggest that NO makes an important contribution during conditioning and acts directly in both the sensory and motor neurons to affect different processes of facilitation at the synapses between them. In addition, they suggest that NO does not come from either the sensory or motor neurons but rather comes from another source, perhaps the L29 interneurons.