{"title":"Embryonic cerebrospinal fluid pressure in fetal mice in utero: External factors pressurize the intraventricular space.","authors":"Koichiro Tsujikawa, Reina Muramatsu, Takaki Miyata","doi":"10.1002/dvdy.70047","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Previous experiments inducing leakage of embryonic cerebrospinal fluid (CSF) suggest the necessity of intraventricular CSF pressure (P<sub>CSF</sub>) for brain morphogenesis. Nevertheless, how embryonic P<sub>CSF</sub> occurs is unclear, especially in utero.</p><p><strong>Results: </strong>Using a Landis water manometer, we measured P<sub>CSF</sub> in fetal mice isolated from the amniotic cavity (P<sub>CSF-ISO</sub>) and found that P<sub>CSF-ISO</sub> rose from 20 Pa at embryonic day (E) 10 to 100-110 Pa at E14-16. At E13, intraventricular injections of ≥3 μL of saline elevated P<sub>CSF-ISO</sub> by ~30%, whereas those of inhibitors of CSF secretion decreased P<sub>CSF-ISO</sub> by ~30%. Shh-mediated cerebral wall expansion did not significantly increase P<sub>CSF-ISO</sub>. Removal of the brain-surrounding contractile tissues decreased P<sub>CSF-ISO</sub> by 80%-90%. We then found that the intraamniotic pressure measured in utero (P<sub>AF-IU</sub>) declined from 2000 Pa at E10 to 500 Pa at E15-18 but was always much greater than P<sub>CSF-ISO</sub>. Direct measurement of P<sub>CSF</sub> in utero (P<sub>CSF-IU</sub>) at E13 and E15 coupled with the measurement of P<sub>CSF-ISO</sub> under hydrostatic pressure loading to mimic P<sub>AF-IU</sub> at various embryonic ages revealed the following relationship: P<sub>CSF-IU</sub> = P<sub>CSF-ISO</sub> + P<sub>AF-IU</sub>.</p><p><strong>Conclusions: </strong>The P<sub>CSF</sub> of mice in utero is influenced by external factors, most strongly by intraamniotic pressure and less strongly by brain-confining tissues.</p>","PeriodicalId":11247,"journal":{"name":"Developmental Dynamics","volume":" ","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Developmental Dynamics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1002/dvdy.70047","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ANATOMY & MORPHOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Previous experiments inducing leakage of embryonic cerebrospinal fluid (CSF) suggest the necessity of intraventricular CSF pressure (PCSF) for brain morphogenesis. Nevertheless, how embryonic PCSF occurs is unclear, especially in utero.
Results: Using a Landis water manometer, we measured PCSF in fetal mice isolated from the amniotic cavity (PCSF-ISO) and found that PCSF-ISO rose from 20 Pa at embryonic day (E) 10 to 100-110 Pa at E14-16. At E13, intraventricular injections of ≥3 μL of saline elevated PCSF-ISO by ~30%, whereas those of inhibitors of CSF secretion decreased PCSF-ISO by ~30%. Shh-mediated cerebral wall expansion did not significantly increase PCSF-ISO. Removal of the brain-surrounding contractile tissues decreased PCSF-ISO by 80%-90%. We then found that the intraamniotic pressure measured in utero (PAF-IU) declined from 2000 Pa at E10 to 500 Pa at E15-18 but was always much greater than PCSF-ISO. Direct measurement of PCSF in utero (PCSF-IU) at E13 and E15 coupled with the measurement of PCSF-ISO under hydrostatic pressure loading to mimic PAF-IU at various embryonic ages revealed the following relationship: PCSF-IU = PCSF-ISO + PAF-IU.
Conclusions: The PCSF of mice in utero is influenced by external factors, most strongly by intraamniotic pressure and less strongly by brain-confining tissues.
期刊介绍:
Developmental Dynamics, is an official publication of the American Association for Anatomy. This peer reviewed journal provides an international forum for publishing novel discoveries, using any model system, that advances our understanding of development, morphology, form and function, evolution, disease, stem cells, repair and regeneration.