Gastrointestinal (GI) dysfunction is commonly reported by people diagnosed with autism spectrum disorder (ASD; autism) but the cause is unknown. Mutations in genes encoding synaptic proteins including Neuroligin‐3 are associated with autism. Mice lacking Neuroligin‐3 (Nlgn3^−/−) have altered brain function, but whether the enteric nervous system (ENS) is altered remains unknown. We assessed for changes in GI structure and function in Nlgn3^−/− mice. We found no significant morphological differences in villus height or crypt depth in the jejunum or colon between wildtype (WT) and Nlgn3^−/− mice. To determine whether deletion of Nlgn3 affects enteric neurons, we stained for neural markers in the myenteric plexus. Nlgn3^−/− mice had similar numbers of neurons expressing the pan‐neuronal marker Hu in the jejunum, proximal mid, and distal colon regions. We also found no differences in the number of neuronal nitric oxide synthase (nNOS+) or calretinin (CalR+) motor neurons and interneurons between WT and Nlgn3^−/− mice. We used ex vivo video imaging analysis to assess colonic motility under baseline conditions and observed faster colonic migrating motor complexes (CMMCs) and an increased colonic diameter in Nlgn3^−/− mice, although CMMC frequency was unchanged. At baseline, CMMCs were faster in Nlgn3^−/− mice compared to WT. Although the numbers of neuronal subsets are conserved in Nlgn3^−/− mice, these findings suggest that Neuroligin‐3 modulates inhibitory neural pathways in the ENS and may contribute to mechanisms underlying GI disorders in autism. Autism Res 2020, 13: 691–701. © 2019 The Authors. Autism Research published by International Society for Autism Research published byWiley Periodicals, Inc.

中文翻译：

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Neuroligin-3基因敲除小鼠的结肠扩张和离体胃肠蠕动改变。

诊断为自闭症谱系障碍（ASD;自闭症）的人通常会报告胃肠道（GI）功能障碍，但原因尚不清楚。编码包括Neuroligin-3在内的突触蛋白的基因突变与自闭症有关。缺乏Neuroligin-3（Nlgn3 ^-/-）的小鼠脑功能已发生改变，但是肠神经系统（ENS）是否发生改变仍是未知的。我们评估了Nlgn3 ^-/-小鼠中GI结构和功能的变化。我们没有发现野生型（WT）和Nlgn3 ^-/-小鼠在空肠或结肠中的绒毛高度或隐窝深度没有明显的形态学差异。为了确定Nlgn3的缺失是否会影响肠神经元，我们对肌间神经丛中的神经标记进行了染色。Nlgn3 ^-/-小鼠在空肠，结肠中部和远端的神经元表达类似泛神经标志物Hu的神经元数量相近。我们还发现野生型和Nlgn3 ^-/-小鼠之间的神经元一氧化氮合酶（nNOS +）或钙调蛋白（CalR +）运动神经元和中间神经元的数量没有差异。我们使用离体视频成像分析来评估基线条件下的结肠运动，并观察到更快的结肠迁移运动复合物（CMMC）和Nlgn3 ^-/-小鼠结肠直径增加，尽管CMMC频率不变。在基线时，与WT相比，Nlgn3 ^-/-小鼠中的CMMC更快。虽然神经元子集的数目在Nlgn3中是保守的^-/-这些发现表明Neuroligin-3调节ENS中的抑制性神经通路，并可能有助于自闭症中胃肠道疾病的潜在机制。Autism Res 2020，13：691-701。©2019作者。由Wiley Periodicals，Inc.出版的国际自闭症研究协会出版的《自闭症研究》。