脊髓胶状质内生长抑素免疫反应阳性结构与一级传入纤维之间的突触连接

SYNAPTIC CONTACTS BETWEEN PRIMARY AFFERENT FIBERS AND SOMATOSTATIN IMMUNOREACTIVE STRUCTURES IN THE SUBSTANTIA GELATINOSA OF THE RAT SPINAL CORD

本文用单纯免疫电镜及免疫电镜与溃变(后根切断术)相结合的方法,研究了一级传入纤维与脊髓胶状质内生长抑素(SOM)阳性结构之间的突触连结。结果在脊髓胶状质内观察到SOM阳性的胞体、轴突、树突及溃变的轴突,以上结构间形成了几种不同类型的突触连结:(1)Ⅰ型或Ⅱ型突触球的中央成份(CⅠ或CⅡ末梢)是溃变的或是SOM免疫反应阳性的,它们与周围的树突形成轴树突触、轴轴突触或树轴突触,其中有一些周围的树突还是SOM阳性的。(2)某些简单的轴突(不参与构成突触球的轴突)呈暗型溃变,并与SOM阳性的树突形成轴树突触。(3)简单的SOM阳性的致密型轴突与含SOM的树突或核周质形成轴树或轴体突触。(4)简单的SOM阳性的亮型轴突与含SOM的树突形成轴树突触。这些突触关系提示脊髓胶状质内SOM阳性树突和胞体可直接从一级传入纤维或脊髓后角固有神经元接受冲动,其中有一些一级传入纤维和脊髓后角固有神经元也是SOM阳性的。这表明在脊髓固有神经元与一级传入纤维之间及脊髓固有神经元本身都存在着自调节突触。本实验结果为SOM参与感觉信息的调节提供了超微结构证据。

Synaptic contacts between primary afferent fibers and somatostatin (SOM) immunoreactive (IR) structures in the substantia gelatiosa of the rat spinal cord have been studied by immunoelectron microscopic technique and combined method of immunocytochemistry and degeneration (dorsal root rhizotomy). The results showed that there were SOM-IR perikarya, axons, dendrites and degenerating axons in the substantia gelatinosa of spinal cord and several kinds of synaptic contacts were observed: (1) Degenerating or SOM-IR primary afferent terminals were commonly observed at the center of type Ⅰ and type Ⅱ synaptic glomeruli where they formed synaptic contacts with surrounding dendrites, some of which were SOM-IR positive; (2) Simple degenerating terminals were presynaptic to a SOM-IR dendrite; (3) Simple dense type SOM-IR axon terminals were presynaptie to a SOM-IR dendrite or perikaryon; (4) Simple light type SOM-IR axon terminals were presynaptic to a SOM-IR dendrite. The above observed synaptic relationships suggested that SOM-IR structures in the substantia gelatinosa of the spinal cord received directly impulses from intrinsical SOM-IR neurons of dorsal horn or from primary afferent fibers, the latter were sometimes SOM-IR too. That means there were autoregulatory synapses between primary afferent fibers and intrinsical neurons of the spinal cord and in intrinsical neurons of spinal cord themselves. It might provide ultrastuctural evidence for the mechanism of SOM in the modulation of sensory information.