Pereda A E, Faber D S
Department of Anatomy and Neurobiology, Medical College of Pennsylvania, Philadelphia, USA.
J Neurosci. 1996 Feb 1;16(3):983-92. doi: 10.1523/JNEUROSCI.16-03-00983.1996.
It was reported previously that repeated brief tetanization of the posterior eight nerve can produce long-term homosynaptic potentiations of the electrotonic and chemical components of the mixed EPSP evoked in the Mauthner cell lateral dendrite by a single stimulus to the nerve. We show here that the same stimulus paradigm can lead, alternatively, to short-term enhancements of both excitatory responses. These transient modifications last for approximately 3 min, with a time course similar to post-tetanic potentiation at chemical synapses. However, a different stimulus pattern that transiently increases the presynaptic calcium concentration, paired-nerve stimuli, does not have any significant effect on electrotonic transmission, whereas it facilitates the chemically mediated EPSP. On the other hand, induction of the short-lasting potentiation of coupling, which depended on the discontinuous or burst-like property of the tetanizing paradigm, required NMDA-receptor activation and was blocked by postsynaptic intradendritic injections of the calcium chelator bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid. The ineffectiveness of presynaptic calcium in potentiating electrotonic coupling likely reflects the involvement of a calcium-dependent regulatory protein in the postsynaptic cell and suggests that hemichannels on the two sides of a gap junction plaque can be modified independently. NMDA-mediated modulation of gap junctions could be widespread, because both types of channels coexist during development and in several mammalian adult central nervous system structures such as hippocampus.
先前有报道称,对后八对神经进行重复短暂强直刺激,可使单个神经刺激在Mauthner细胞侧树突诱发的混合兴奋性突触后电位(EPSP)的电紧张成分和化学成分产生长期的同突触增强。我们在此表明,相同的刺激模式可交替导致两种兴奋性反应的短期增强。这些短暂的改变持续约3分钟,其时程类似于化学突触处的强直后增强。然而,一种短暂增加突触前钙浓度的不同刺激模式,即配对神经刺激,对电紧张性传递没有任何显著影响,而它会促进化学介导的EPSP。另一方面,依赖于强直刺激模式的不连续或爆发样特性的耦合的短暂增强的诱导需要NMDA受体激活,并被突触后树突内注射钙螯合剂双(2-氨基苯氧基)乙烷-N,N,N',N'-四乙酸所阻断。突触前钙在增强电紧张性耦合方面的无效性可能反映了突触后细胞中一种钙依赖性调节蛋白的参与,并表明缝隙连接斑块两侧的半通道可以独立修饰。NMDA介导的缝隙连接调节可能很普遍,因为这两种类型的通道在发育过程中以及在几种哺乳动物成年中枢神经系统结构(如海马体)中共存。