Cattaert D, El Manira A
Laboratoire Neurobiologie et Mouvements, Centre National de la Recherche Scientifique, 13402 Marseille Cedex 20, France.
J Neurosci. 1999 Jul 15;19(14):6079-89. doi: 10.1523/JNEUROSCI.19-14-06079.1999.
Primary afferent depolarizations (PADs) are associated with presynaptic inhibition in both vertebrates and invertebrates. In the present study, we have used both anatomical and electrophysiological techniques to analyze the relative importance of shunting mechanisms versus sodium channel inactivation in mediating the decrease of action potential amplitude, and thereby presynaptic inhibition. Experiments were performed in sensory afferents of a stretch receptor in an in vitro preparation of the crayfish. Lucifer yellow intracellular labeling of sensory axons combined with GABA immunohistochemistry revealed close appositions between GABA-immunoreactive (ir) fibers and sensory axons. Most contacts were located on the main axon at the entry zone of the ganglion, close to the first branching point within the ganglion. By comparison, the output synapses of sensory afferents to target neurons were located on distal branches. The location of synaptic inputs mediating spontaneous PADs was also determined electrophysiologically by making dual intracellular recordings from single sensory axons. Inputs generating PADs appear to occur around the first axonal branching point, in agreement with the anatomical data. In this region, small PADs (3-15 mV) produced a marked reduction of action potential amplitude, whereas depolarization of the membrane potential by current injection up to 15 mV had no effect. These results suggest that the decrease of the amplitude of action potentials by single PADs results from a shunting mechanism but does not seem to involve inactivation of sodium channels. Our results also suggest that GABAergic presynaptic inhibition may act as a global control mechanism to block transmission through certain reflex pathways.
初级传入去极化（PADs）在脊椎动物和无脊椎动物中均与突触前抑制相关。在本研究中，我们运用解剖学和电生理学技术，分析了分流机制与钠通道失活在介导动作电位幅度降低进而介导突触前抑制方面的相对重要性。实验在小龙虾体外制备的牵张感受器的感觉传入纤维中进行。感觉轴突的荧光黄细胞内标记与GABA免疫组织化学相结合，揭示了GABA免疫反应性（ir）纤维与感觉轴突之间的紧密毗邻关系。大多数接触点位于神经节入口区域的主轴突上，靠近神经节内的第一个分支点。相比之下，感觉传入纤维与靶神经元的输出突触位于远端分支上。通过对单个感觉轴突进行双细胞内记录，还从电生理学角度确定了介导自发性PADs的突触输入位置。产生PADs的输入似乎发生在第一个轴突分支点周围，这与解剖学数据一致。在该区域，小幅度的PADs（3 - 15 mV）可使动作电位幅度显著降低，而通过电流注入使膜电位去极化高达15 mV则没有影响。这些结果表明，单个PADs引起的动作电位幅度降低是由分流机制导致的，但似乎不涉及钠通道失活。我们的结果还表明，GABA能突触前抑制可能作为一种全局控制机制，通过某些反射途径阻断信号传递。
