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首页> 外文期刊>The European Journal of Neuroscience >Disabled‐1 dorsal horn spinal cord neurons co‐express Lmx1b and function in nociceptive circuits
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Disabled‐1 dorsal horn spinal cord neurons co‐express Lmx1b and function in nociceptive circuits

机译：残疾人-1背角脊髓神经元Co-Express LMX1B和在伤害电路中的功能

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摘要

The Reelin‐signaling pathway is essential for correct neuronal positioning within the central nervous system. Mutant mice with a deletion of Reelin, its lipoprotein receptors, or its intracellular adaptor protein Disabled‐1 (Dab1), exhibit nociceptive abnormalities: thermal (heat) hyperalgesia and reduced mechanical sensitivity. To determine dorsal horn alterations associated with these nociceptive abnormalities, we first characterized the correctly positioned Dab1 neurons in wild‐type and mispositioned neurons in Reelin‐signaling pathway mutant lumbar spinal cord. Using immunofluorescence, we found that 70% of the numerous Dab1 neurons in Reln+/+ laminae I–II and 67% of those in the lateral reticulated area and lateral spinal nucleus (LSN) co‐express the LIM‐homeobox transcription factor 1 beta (Lmx1b), an excitatory glutamatergic neuron marker. Evidence of Dab1‐ and Dab1‐Lmx1b neuronal positioning errors was found within the isolectin B4 terminal region of Reln?/? lamina IIinner and in the lateral reticulated area and LSN, where about 50% of the Dab1‐Lmx1b neurons are missing. Importantly, Dab1‐Lmx1b neurons in laminae I–II and the lateral reticulated area express Fos after noxious thermal or mechanical stimulation and thus participate in these circuits. In another pain relevant locus – the lateral cervical nucleus (LCN), we also found about a 50% loss of Dab1‐Lmx1b neurons in Reln?/? mice. We suggest that extensively mispositioned Dab1 projection neurons in the lateral reticulated area, LSN, and LCN and the more subtle positioning errors of Dab1 interneurons in laminae I–II contribute to the abnormalities in pain responses found in Reelin‐signaling pathway mutants
机译：Reelin-Signaling路径对于校正中枢神经系统内的正确神经元定位是必不可少的。突变小鼠缺失Reelin，其脂蛋白受体或其细胞内接合蛋白残疾 - 1（DAB1），表现出伤害异常：热（热）痛觉痛觉和机械敏感性降低。为了确定与这些伤害异常相关的背孔改变，我们首先在Reelin-Signal途径突变腰椎脐带中以野生型和错误定位的神经元进行正确定位的DAB1神经元。使用免疫荧光，我们发现，Reln + / +薄膜I-II中的众多DAB1神经元的70％和横向网状区域和侧向脊柱核（LSN）中的67％共表达LiM- Homeobox转录因子1β（ LMX1B），一种兴奋性谷氨酸神经神经元标记物。在Reln的Isolectin B4末端区域内发现DAB1和DAB1-LMX1B神经元定位误差的证据？/？ Lamina IINNER和横向网状区域和LSN，其中缺少约50％的DAB1-LMX1B神经元。重要的是，在薄层I-II中的DAB1-LMX1B神经元和横向网状区域以后的热或机械刺激之后表达FOS，从而参与这些电路。在另一个疼痛相关轨迹 - 侧颈核（LCN）中，我们还发现Reln中的DAB1-LMX1B神经元的损失约为50％？/？老鼠。我们建议在横向网状面积，LSN和LCN中具有广泛性的DAB1投影神经元以及薄层II-II中DAB1 Interneurons的更细微定位误差有助于Reelin-信号通路突变体中发现的疼痛反应的异常

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