Maternal caffeine consumption during pregnancy does not affect preimplantation development but delays early postimplantation growth in rat embryos

1999 ◽  
Vol 11 (5) ◽  
pp. 211 ◽  
Author(s):  
Anita Jacombs ◽  
Irina Pollard ◽  
John Ryan ◽  
Anne Loupis
Keyword(s):  
Embryo Development ◽  
Neural Tube ◽  
Preimplantation Embryo ◽  
Neural Tube Closure ◽  
Preimplantation Embryos ◽  
Fetal Life ◽  
Stage Of Development ◽  
Somite Number ◽  
Caffeine Exposure ◽  
Tube Closure

Models for studying prenatal drug-induced intrauterine growth retardation (IUGR) have, without exception, measured growth-related factors in the postimplantation embryo, fetus or neonate. Therefore, it is not known whether effects of drug exposure on growth and metabolism begin early in the preimplantation embryo, or whether IUGR is exclusively a postimplantation phenomenon. The present study investigates whether caffeine, a drug known to induce a dose-dependent fetal IUGR, affects embryo development before and/or after implantation or is exclusively a fetal phenomenon. Preimplantation embryo assessment (with treatment from Days 2 to 4 of pregnancy) included glucose utilization, cell number evaluation and stage of development (morula to hatched blastocyst); whereas, postimplantation embryo assessment (treatment from Days 2 to 10, 10.5 or 11 of pregnancy) included somite number evaluation and extent of neural tube closure, as seen using scanning electron microscopy. Comparing control preimplantation embryos with those exposed to 30 and 60 mg kg –1 caffeine did not reveal any effects of caffeine exposure, as assessed on Day 5 of gestation. However, postimplantation embryo development assessed on Day 12 of gestation revealed that caffeine exposure of 15 and 30 mg kg –1 significantly reduced, at both dosage levels, somite number and the extent of neural tube closure. In addition, comparisons of control and experimental groups revealed that in the high-dose caffeine group the forebrain cavity was significantly enlarged and bounded by a reduced, irregularly aligned neuroepithelium. The findings suggest that IUGR is a phenomenon first identifiable during late postimplantation embryogenesis and continues in fetal life.

Inhibition of MTOR signaling impairs rat embryo organogenesis by affecting folate availability

Reproduction ◽  
2021 ◽  
Vol 161 (4) ◽  
pp. 365-373
Author(s):  
Romina Higa ◽  
Fredrick J Rosario ◽  
Theresa L Powell ◽  
Thomas Jansson ◽  
Alicia Jawerbaum
Keyword(s):  
Folic Acid ◽  
Embryo Development ◽  
Neural Tube ◽  
Folic Acid Supplementation ◽  
Mtor Signaling ◽  
Neural Tube Closure ◽  
Folate Supplementation ◽  
Mtor Inhibition ◽  
Resorption Rate ◽  
Tube Closure

Mechanistic target of rapamycin (MTOR) is essential for embryo development by acting as a nutrient sensor to regulate cell growth, proliferation and metabolism. Folate is required for normal embryonic development and it was recently reported that MTOR functions as a folate sensor. In this work, we tested the hypothesis that MTOR functions as a folate sensor in the embryo and its inhibition result in embryonic developmental delay affecting neural tube closure and that these effects can be rescued by folate supplementation. Administration of rapamycin (0.5 mg/kg) to rats during early organogenesis inhibited embryonic ribosomal protein S6, a downstream target of MTOR Complex1, markedly reduced embryonic folate incorporation (−84%, P < 0.01) and induced embryo developmental impairments, as shown by an increased resorption rate, reduced embryo somite number and delayed neural tube closure. These alterations were prevented by folic acid administered to the dams. Differently, although an increased rate of embryonic rotation defects was observed in the rapamycin-treated dams, this alteration was not prevented by maternal folic acid supplementation. In conclusion, MTOR inhibition during organogenesis in the rat resulted in decreased folate levels in the embryo, increased embryo resorption rate and impaired embryo development. These data suggest that MTOR signaling influences embryo folate availability, possibly by regulating the transfer of folate across the maternal–embryonic interface.

The role of microfilaments in cranial neurulation in rat embryos: effects of short-term exposure to cytochalasin D

Development ◽  
1985 ◽  
Vol 88 (1) ◽  
pp. 333-348
Author(s):  
Gillian Morriss-Kay ◽  
Fiona Tuckett
Keyword(s):  
Neural Tube ◽  
Amorphous Material ◽  
Cytochalasin D ◽  
Neural Tube Closure ◽  
Rat Embryos ◽  
Stage Of Development ◽  
Microfilament Bundles ◽  
Short Term Exposure ◽  
Tube Closure

During the late stages of cranial neurulation in mammalian embryos, the neural epithelium becomes concave. A thick subapical band of microfilament bundles, attached to junctions which are both vertical and horizontal in orientation, can be seen by TEM. Prior to this the neural epithelium is first biconvex and then V-shaped in transverse section, microfilament bundles are absent, and the subapical junctions are only vertical in orientation. In order to determine the role of microfilaments in cranial neurulation, rat embryos were exposed to cytochalasin D (0·15 μg ml−1) for lh at three stages of development: convex neural fold stage, early concave (prior to midline apposition at the forebrain/midbrain junction: ‘preapposition’) and later concave (‘postapposition’). They were subsequently washed and cultured in addition-free medium for 5,12, 24 or 36h, then examined alive and by LM, TEM, or SEM. The degree of neural fold collapse varied with the stage of development: at the convex stage there was only slight opening out of the neural groove; early concave (preapposition) neural folds collapsed laterally to a horizontal position; later concave (postapposition) neural folds showed widening of the midbrain/hindbrain neuropore and slight neuroepithelial eversion at the anterior neuropore. Neural epithelium which had been concave prior to cytochalasin D treatment changed in structure so that the cells were broader and shorter; most of the subapical junctions were vertical in orientation, and microfilament bundles were represented either as a mass of amorphous material adjacent to the junctions, or as separated and broken filaments. Re-elevation of neural folds in ‘recovery’ cultures was accompanied by regeneration of apical microfilament bundles and horizontal junctions. Embryos which had been exposed to cytochalasin D at the convex or later concave stage of cranial neural fold development were able to complete cranial neural tube closure; none of the early-concave-stage embryos achieved apposition at the forebrain/midbrain junction, and all had major cranial neural tube defects. The results suggest that contraction of apical microfilament bundles plays an essential role in elevation of the neural folds and in the generation of concave curvature during the later stages of cranial neurulation. During the convex neural fold stage, microfilaments are important in maintaining neuroepithelial apposition in the neural groove, but are not crucial to maintenance of the convex shape. Successful formation and maintenance of the forebrain/midbrain apposition point at the appropriate time is considered to be essential for subsequent brain tube closure.

Whole Rat Embryos Require Methionine for Neural Tube Closure when Cultured on Cow Serum

1989 ◽  
Vol 119 (11) ◽  
pp. 1716-1725 ◽  
Author(s):  
Caroline N. D. Coelho ◽  
James A. Weber ◽  
Norman W. Klein ◽  
Willard G. Daniels ◽  
Thomas A Hoagland
Keyword(s):  
Neural Tube ◽  
Neural Tube Closure ◽  
Rat Embryos ◽  
Tube Closure
Sign in / Sign up

Export Citation Format

Share Document