Catarsi S, Drapeau P
Centre for Research in Neuroscience, McGill University, Montreal, Quebec, Canada.
Neuron. 1992 Feb;8(2):275-81. doi: 10.1016/0896-6273(92)90294-n.
Pressure-sensitive (P) neurons contacted by serotonergic Retzius (R) neurons of the leech in culture selectively reduce a protein kinase C (PKC)-dependent cation response to serotonin and are innervated by the inhibitory, Cl(-)-dependent synapse seen in vivo. We have examined whether the reduction of extrasynaptic cation channel modulation is due to changes in sensitivity of the channels to second messenger. In inside-out membrane patches from single, uncontacted P cells in culture, cation channel activity was increased by rat brain PKC and cofactors. In contrast, the activity of cation channels in patches isolated from P cells paired with R cells was unaffected by PKC. These results demonstrate the loss of extrasynaptic channel modulation by PKC during synapse formation.
在培养物中，受水蛭5-羟色胺能Retzius（R）神经元接触的压力敏感（P）神经元选择性降低对5-羟色胺的蛋白激酶C（PKC）依赖性阳离子反应，并由体内所见的抑制性、Cl⁻依赖性突触支配。我们已经研究了突触外阳离子通道调节的降低是否是由于通道对第二信使的敏感性变化所致。在培养的单个未接触的P细胞的内翻膜片中，大鼠脑PKC和辅助因子可增加阳离子通道活性。相反，从与R细胞配对的P细胞分离的膜片中，阳离子通道的活性不受PKC影响。这些结果证明了突触形成过程中PKC对突触外通道调节的丧失。
