Lessmann V, Dietzel I D
Lehrstuhl für Molekulare Neurobiochemie, Ruhr-Universität Bochum, F.R.G.
Neuroscience. 1995 Aug;67(3):525-9. doi: 10.1016/0306-4522(95)00123-z.
Postsynaptic Ca2+ signals are a precondition for many types of synapse modification, including long-term potentiation. Here we describe a postsynaptic mechanism that augments synaptic currents at the serotonergic Retzius-P cell synapse of the leech. Depolarizations large enough to elicit Ca2+ currents evoked an increase in the amplitude of serotonin-activated Cl- currents in isolated embryonic neurons as well as at the Retzius-P cell synapse. The effect on embryonic whole cell currents lasted for up to one hour and was abolished in solutions containing Cd2+ as a Ca2+ channel blocker. Hence, Ca2+ influx into the postsynaptic neuron may be a common step regulating the plasticity of various vertebrate as well as invertebrate synapses.
突触后钙离子信号是包括长时程增强在内的多种突触修饰类型的前提条件。在此，我们描述一种突触后机制，该机制可增强水蛭5-羟色胺能Retzius-P细胞突触处的突触电流。足以引发钙离子电流的去极化，在分离的胚胎神经元以及Retzius-P细胞突触处，诱发了5-羟色胺激活的氯离子电流幅度增加。对胚胎全细胞电流的影响持续长达一小时，并且在含有作为钙离子通道阻滞剂的镉离子的溶液中被消除。因此，钙离子流入突触后神经元可能是调节各种脊椎动物以及无脊椎动物突触可塑性的一个共同步骤。
