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Gastrointestinal tract abnormalities induced by prenatal valproic Acid exposure in rat offspring
Ji-Woon Kim1, Chang Soon Choi1, Ki Chan Kim1
1Department of Neuroscience, School of Medicine and Center for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Korea.
Insights
Prenatal exposure to valproic acid (VPA) in rats induced autism spectrum disorder (ASD) and gastrointestinal (GI) issues. VPA altered GI structure and reduced motility, offering insights into ASD-related GI complications.
Area of Science:
- Neuroscience
- Developmental Biology
- Gastroenterology
Background:
- Valproic acid (VPA) exposure in utero is a known risk factor for autism spectrum disorder (ASD).
- ASD patients frequently experience gastrointestinal (GI) problems, but the underlying mechanisms remain unclear.
- Investigating the GI tract in VPA-induced ASD animal models is crucial for understanding these comorbidities.
Purpose of the Study:
- To examine the gross structure and motility of the gastrointestinal (GI) tract in a valproic acid (VPA)-induced animal model of autism spectrum disorder (ASD).
- To identify specific structural changes in the GI tract associated with prenatal VPA exposure.
- To assess the functional impact of VPA exposure on GI motility in the offspring.
Main Methods:
- Pregnant Sprague-Dawley rats were injected with VPA or phosphate-buffered saline (PBS) on embryonic day 12.
- Offspring were analyzed at 4 weeks of age for gross GI structure and microscopic changes.
- High-resolution microscopy and hematoxylin and eosin (H&E) staining were used to evaluate cellular morphology.
- GI motility was assessed in the VPA-exposed and control groups.
Main Results:
- VPA exposure reduced the thickness of the stomach and ileum tunica mucosa and tunica muscularis.
- Microscopic analysis revealed atrophy of parietal and chief cells in the stomach and absorptive cells in the ileum.
- Epithelial cell staining was decreased in H&E-stained ileum sections.
- Prenatal VPA exposure resulted in decreased GI tract motility in the rat offspring.
Conclusions:
- The VPA-induced ASD rat model exhibits significant abnormalities in GI tract structure and function.
- These findings suggest a link between prenatal VPA exposure, altered GI morphology, and impaired GI motility.
- This model provides valuable insights into the pathophysiology of GI complications associated with ASD phenotypes.
Abstract:
In-utero exposure to valproic acid (VPA) has been known as a potent inducer of autism spectrum disorder (ASD), not only in humans, but also in animals. In addition to the defects in communication and social interaction as well as repetitive behaviors, ASD patients usually suffer from gastrointestinal (GI) problems. However, the exact mechanism underlying these disorders is not known. In this study, we examined the gross GI tract structure and GI motility in a VPA animal model of ASD. On embryonic day 12 (E12), 4 pregnant Sprague-Dawley (SD) rats were subcutaneously injected with VPA (400 mg/kg) in the treatment group, and with phosphate buffered saline (PBS) in the control group; the resulting male offspring were analyzed at 4 weeks of age. VPA exposure decreased the thickness of tunica mucosa and tunica muscularis in the stomach and ileum. Other regions such as duodenum, jejunum, and colon did not show a significant difference. In high-resolution microscopic observation, atrophy of the parietal and chief cells in the stomach and absorptive cells in the ileum was observed. In addition, decreased staining of the epithelial cells was observed in the hematoxylin and eosin (H&E)-stained ileum section. Furthermore, decreased motility in GI tract was also observed in rat offspring prenatally exposed to VPA. However, the mechanism underlying GI tract defects in VPA animal model as well as the association between abnormal GI structure and function with ASD is yet to be clearly understood. Nevertheless, the results from the present study suggest that this VPA ASD model undergoes abnormal changes in the GI structure and function, which in turn could provide beneficial clues pertaining to the pathophysiological relevance of GI complications and ASD phenotypes.
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