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Neurogenic bowel is a major cause of morbidity in patients affected by spina bifida, but it is unknown whether the gastrointestinal (\n                      <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>\n                      ) tract is affected in other types of\n                      <jats:styled-content style=\"fixed-case\">NTDs<\/jats:styled-content>\n                      . An absolute requirement for\n                      <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>\n                      motility is the enteric nervous system (\n                      <jats:styled-content style=\"fixed-case\">ENS<\/jats:styled-content>\n                      ) located within the walls of the\n                      <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>\n                      tract. Enteric neurons coalesce into circumferential stripes throughout embryonic, fetal, and early postnatal development, and this gradual organization of the\n                      <jats:styled-content style=\"fixed-case\">ENS<\/jats:styled-content>\n                      into enteric neuronal stripes correlates with the emergence of neurogenic\n                      <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>\n                      motility. We hypothesized that\n                      <jats:styled-content style=\"fixed-case\">NTDs<\/jats:styled-content>\n                      are associated with changes in\n                      <jats:styled-content style=\"fixed-case\">ENS<\/jats:styled-content>\n                      organization that correlate with specific\n                      <jats:styled-content style=\"fixed-case\">GI<\/jats:styled-content>\n                      motility defects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used prenatal valproic acid (\n                      <jats:styled-content style=\"fixed-case\">VPA<\/jats:styled-content>\n                      ) exposure to induce exencephaly, a cranial\n                      <jats:styled-content style=\"fixed-case\">NTD<\/jats:styled-content>\n                      , in fetal mice. We used immunohistochemistry, high resolution confocal imaging, and ex\u00a0vivo motility assays to assess enteric neuronal stripes and gastrointestinal motility in fetuses with a\n                      <jats:styled-content style=\"fixed-case\">VPA<\/jats:styled-content>\n                      \u2010induced\n                      <jats:styled-content style=\"fixed-case\">NTD<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>GI tracts from fetuses with a VPA\u2010induced NTD contain blood. Structurally, the enteric neuronal stripes are thinner with a narrower interstripe distance, leading to an increased number of stripes. Functionally, GI motility is abnormal, with increased contraction frequency and increased length of contractile segments.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions and Inferences<\/jats:title>\n                    <jats:p>ENS organization and GI motility are disrupted in mouse fetuses with a VPA\u2010induced NTD. This has important implications for our understanding of neurogenic bowel in central nervous system diseases such as spina bifida.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/nmo.70368","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T05:38:08Z","timestamp":1780465088000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Abnormal Enteric Nervous System Organization and Gastrointestinal Motility in Mice With Valproic Acid\u2010Induced Neural Tube Defects"],"prefix":"10.1111","volume":"38","author":[{"given":"Gabrielle R.","family":"Barsh","sequence":"first","affiliation":[{"name":"Department of Neurology Stanford University School of Medicine  Stanford California USA"},{"name":"Wu Tsai Neurosciences Institute Stanford University  Stanford California 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