Drapeau P
Centre for Research in Neuroscience, Montreal General Hospital, Quebec, Canada.
Neuron. 1990 Jun;4(6):875-82. doi: 10.1016/0896-6273(90)90140-b.
When serotonergic Retzius (R) neurons of the leech contact pressure-sensitive (P) neurons in culture, P cells selectively lose a protein kinase C-dependent cationic response to serotonin and the R cell reforms the inhibitory, chloride-dependent synapse seen in vivo. In P cells not contacted by R cells, cell-attached patches contained single cation channels sensitive to serotonin and phorbol ester with characteristic properties and high incidence (present in about one-half of the patches). P cells paired with R cells had a cation channel with similar biophysical properties and incidence, but channel activity was not stimulated by serotonin and phorbol ester. These results suggest that the early clearing of the non-synaptic (excitatory) response to serotonin is due to the loss of activation by protein kinase C (and not the number) of cation channels as a prelude to inhibitory synapse formation.
当水蛭的5-羟色胺能Retzius（R）神经元在培养物中与压力敏感（P）神经元接触时，P细胞会选择性地丧失对5-羟色胺的蛋白激酶C依赖性阳离子反应，并且R细胞会重新形成在体内可见的抑制性、氯离子依赖性突触。在未与R细胞接触的P细胞中，细胞贴附式膜片包含对5-羟色胺和佛波酯敏感的单个阳离子通道，这些通道具有特征性特性且发生率很高（约一半的膜片中存在）。与R细胞配对的P细胞具有生物物理特性和发生率相似的阳离子通道，但5-羟色胺和佛波酯不会刺激通道活性。这些结果表明，对5-羟色胺的非突触性（兴奋性）反应的早期清除是由于作为抑制性突触形成前奏的阳离子通道蛋白激酶C激活的丧失（而非数量的丧失）。
