DeMill Colin M, Delaney Kerry R
Department of Biology, Simon Fraser University, Burnaby, British Columbia V5A 1S6, Canada.
J Exp Biol. 2005 Jun;208(Pt 11):2135-45. doi: 10.1242/jeb.01633.
Action potential-mediated calcium (Ca) entry into excitor nerve terminal boutons during presynaptic inhibition and the effects of co-activation of the inhibitor on the kinetics of muscle contraction were studied at crayfish claw opener muscle. Inhibition reduced postsynaptic excitatory junction potentials (EJPs) below the threshold to initiate contraction. Upon cessation of inhibition, EJP amplitudes immediately increased several-fold due to the build-up of presynaptic facilitation during inhibition. Consequently, muscle contraction was initiated more rapidly after a period of inhibitor-excitor coactivation. Presynaptic inhibition reduced Ca entry into presynaptic excitor terminal boutons (range 0-50%, mean +/-s.e.m.=20+/-1%, N=122 terminals; 12 preparations) and reduced the EJP amplitude (range 30-70%, mean +/- s.e.m.=51+/-2%, N=27 cells). The decline in the EJP was proportional to the reduction of Ca influx raised to the power of 2.8. Since presynaptic inhibition reduces the number of Ca channels opened by an action potential, our data suggest cooperativity between Ca channel microdomains to initiate vesicle fusion at this synapse. The amount of inhibition of Ca influx into an excitor bouton was not correlated with either the distance to the closest inhibitor bouton or the main excitor branch, although slightly more inhibition was seen for excitor boutons on tertiary versus secondary branches. Unlike inhibitor axon stimulation, bath application of GABA caused inhibition of Ca influx that steadily increased from proximal to distal terminal boutons on a branch. We propose a model where presynaptic inhibition causes localized shunting of an actively propagated action potential in the vicinity of release sites, which can recover its amplitude outside the shunted region.
在小龙虾爪开肌上，研究了突触前抑制期间动作电位介导的钙（Ca）进入兴奋性神经末梢终扣的情况，以及抑制剂共激活对肌肉收缩动力学的影响。抑制作用使突触后兴奋性接头电位（EJP）降低至引发收缩的阈值以下。抑制停止后，由于抑制期间突触前易化的积累，EJP幅度立即增加了几倍。因此，在一段时间的抑制剂 - 兴奋性神经元共激活后，肌肉收缩启动得更快。突触前抑制减少了Ca进入突触前兴奋性终末终扣（范围0 - 50%，平均值±标准误=20±1%，N = 122个终扣；12个标本），并降低了EJP幅度（范围30 - 70%，平均值±标准误=51±2%，N = 27个细胞）。EJP的下降与Ca内流减少至2.8次方成正比。由于突触前抑制减少了动作电位打开的Ca通道数量，我们的数据表明Ca通道微区之间存在协同作用，以在该突触处启动囊泡融合。进入兴奋性终扣的Ca内流抑制量与到最近的抑制性终扣的距离或主要兴奋性分支均无关，尽管在三级分支上的兴奋性终扣比二级分支上的兴奋性终扣观察到稍多的抑制。与抑制性轴突刺激不同，浴槽中应用GABA导致Ca内流受到抑制，这种抑制从分支上的近端终扣到远端终扣稳步增加。我们提出了一个模型，其中突触前抑制导致释放位点附近主动传播的动作电位发生局部分流，该动作电位可在分流区域外恢复其幅度。
