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首页> 外文期刊>The European Journal of Neuroscience >Plasticity of somatostatin and somatostatin sst2A receptors in the rat dentate gyrus during kindling epileptogenesis.
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Plasticity of somatostatin and somatostatin sst2A receptors in the rat dentate gyrus during kindling epileptogenesis.

机译：点燃癫痫发生过程中大鼠齿状回中生长抑素和生长抑素sst2A受体的可塑性。

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Abstract Increasing evidence suggests that somatostatin may control neuronal excitability during epileptogenesis. In the hippocampus, sst2A receptors are likely to mediate somatostatin inhibitory actions but little is known about their status in kindled tissues. In the present study, sst2A receptor and somatostatin immunoreactivity were examined by confocal microscopy in the hippocampus during and after kindling acquisition. In control rats, somatostatin-positive axon terminals were mainly found in the stratum lacunosum moleculare of CA1 area and in the outer molecular layer of the dentate gyrus. sst2A receptor immunoreactivity was diffusely distributed in the strata radiatum and oriens of CA1 and in the stratum moleculare of the dentate gyrus. Immunogold electron microscopy revealed that sst2A receptors were predominantly localized postsynaptically, at the plasma membrane of dendritic shafts and spines of principal neurons. During kindling epileptogenesis, qualitative and semiquantitative analysis revealed a progressive decrease of sst2A immunoreactivity in the outer molecular layer, which was spatially associated with an increase in somatostatin immunoreactivity. No obvious changes in sst2A receptor immunoreactivity were observed in other hippocampal subfields. These results suggest that the decrease of sst2A receptor immunoreactivity in the outer molecular layer reflects receptor down-regulation in distal dendrites of granule cells in response to chronic somatostatin release. Because the sst2A receptor appears to mediate anticonvulsant and antiepileptogenic effects of somatostatin, this may represent a pivotal mechanism contributing to epileptogenesis.
机译：摘要越来越多的证据表明生长抑素可能在癫痫发生过程中控制神经元兴奋性。在海马中，sst2A受体可能介导生长抑素抑制作用，但对于它们在点燃组织中的状态知之甚少。在本研究中，共聚焦显微镜检查了点燃过程中和点燃后海马的sst2A受体和生长抑素的免疫反应性。在对照大鼠中，生长抑素阳性的轴突末端主要在CA1区的腔纹层分子和齿状回的外分子层中发现。 sst2A受体的免疫反应性广泛分布在CA1的放射线层和东方以及齿状回的层分子中。免疫金电子显微镜检查显示，sst2A受体主要位于突触后，位于树突干和主要神经元棘的质膜上。在点燃癫痫发生过程中，定性和半定量分析显示外分子层中sst2A免疫反应性逐渐降低，这与生长抑素免疫反应性的增加在空间上相关。在其他海马亚域中未观察到sst2A受体免疫反应性的明显变化。这些结果表明外分子层中sst2A受体免疫反应性的降低反映了响应于慢性生长抑素释放的颗粒细胞远端树突中受体的下调。因为sst2A受体似乎介导生长抑素的抗惊厥和抗癫痫作用，所以这可能是促成癫痫发生的关键机制。

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