Park J H, Straub V A, O'Shea M
Sussex Centre for Neuroscience, School of Biological Sciences, University of Sussex, Brighton, East Sussex, BN1 9QG, United Kingdom.
J Neurosci. 1998 Jul 15;18(14):5463-76. doi: 10.1523/JNEUROSCI.18-14-05463.1998.
Nitric oxide (NO) is recognized as a signaling molecule in the CNS where it is a candidate retrograde neurotransmitter. Here we provide direct evidence that NO mediates slow excitatory anterograde transmission between the NO synthase (NOS)-expressing B2 neuron and an NO-responsive follower neuron named B7nor. Both are motoneurons located in the buccal ganglia of the snail Lymnaea stagnalis where they participate in feeding behavior. Transmission between B2 and B7nor is blocked by inhibiting NOS and is suppressed by extracellular scavenging of NO. Furthermore, focal application of NO to the cell body of the B7nor neuron causes a depolarization that mimics the effect of B2 activity. The slow interaction between the B2 and B7nor neurons can be re-established when the two neurons are cocultured, and it shows the same susceptibility to NOS inhibition and NO scavenging. In cell culture we have also examined spatial aspects of NO signaling. We show that before the formation of an anatomical connection, the presynaptic neuron can cause depolarizing potentials in the follower neuron at distances up to 50 micro(m). The strength of the interaction increases when the distance between the cells is reduced. Our results suggest that NO can function as both a synaptic and a nonsynaptic signaling molecule.
一氧化氮（NO）在中枢神经系统中被认为是一种信号分子，它是一种逆行神经递质的候选分子。在此我们提供直接证据，表明NO介导了表达一氧化氮合酶（NOS）的B2神经元与名为B7nor的NO反应性跟随神经元之间的缓慢兴奋性顺行传递。两者都是位于椎实螺颊神经节中的运动神经元，它们参与进食行为。B2和B7nor之间的传递可通过抑制NOS而阻断，并可通过细胞外清除NO而受到抑制。此外，向B7nor神经元的细胞体局部施加NO会引起去极化，这模拟了B2活动的效果。当两个神经元共培养时，B2和B7nor神经元之间的缓慢相互作用可以重新建立，并且它对NOS抑制和NO清除表现出相同的敏感性。在细胞培养中，我们还研究了NO信号传导的空间方面。我们表明，在解剖学连接形成之前，突触前神经元可以在距离跟随神经元高达50微米的距离处引起去极化电位。当细胞之间的距离减小时，相互作用的强度会增加。我们的结果表明，NO既可以作为突触信号分子，也可以作为非突触信号分子发挥作用。
