Most cited article - PubMed ID 28937253
Sirt1 mediates improvement in cognitive defects induced by focal cerebral ischemia following hyperbaric oxygen preconditioning in rats
The healthy development of the fetus depends on the exact course of pregnancy and delivery. Therefore, prenatal hypoxia remains between the greatest threats to the developing fetus. Our study aimed to assess the impact of prenatal hypoxia on postnatal development and behavior of the rats, whose mothers were exposed to hypoxia (10.5 % O2) during a critical period of brain development on GD20 for 12 h. This prenatal insult resulted in a delay of sensorimotor development of hypoxic pups compared to the control group. Hypoxic pups also had lowered postnatal weight which in males persisted up to adulthood. In adulthood, hypoxic males showed anxiety-like behavior in the OF, higher sucrose preference, and lower levels of grimace scale (reflecting the degree of negative emotions) in the immobilization chamber compared to the control group. Moreover, hypoxic animals showed hyperactivity in EPM and LD tests, and hypoxic females had reduced sociability compared to the control group. In conclusion, our results indicate a possible relationship between prenatal hypoxia and changes in sociability, activity, and impaired emotion regulation in ADHD, ASD, or anxiety disorders. The fact that changes in observed parameters are manifested mostly in males confirms that male sex is more sensitive to prenatal insults.
- MeSH
- Acid-Base Equilibrium MeSH
- Maze Learning MeSH
- Behavior, Animal * MeSH
- Gestational Age MeSH
- Fetal Hypoxia complications physiopathology MeSH
- Disease Models, Animal MeSH
- Motor Activity MeSH
- Rats, Wistar MeSH
- Food Preferences MeSH
- Sensorimotor Cortex growth & development MeSH
- Sex Factors MeSH
- Social Interaction MeSH
- Pregnancy MeSH
- Reflex, Startle MeSH
- Age Factors MeSH
- Prenatal Exposure Delayed Effects * MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Perinatal hypoxia is still one of the greatest threats to the newborn child, even in developed countries. However, there is a lack of works which summarize up-to-date information about that huge topic. Our review covers a broader spectrum of recent results from studies on mechanisms leading to hypoxia-induced injury. It also resumes possible primary causes and observed behavioral outcomes of perinatal hypoxia. In this review, we recognize two types of hypoxia, according to the localization of its primary cause: environmental and placental. Later we analyze possible pathways of prenatal hypoxia-induced injury including gene expression changes, glutaminergic excitatory damage (and a role of NMDA receptors in it), oxidative stress with ROS and RNS production, inflammation and apoptosis. Moreover, we focus on the impact of these pathophysiological changes on the structure and development of the brain, especially on its regions: corpus striatum and hippocampus. These brain changes of the offspring lead to impairments in their postnatal growth and sensorimotor development, and in their motor functions, activity, emotionality and learning ability in adulthood. Later we compare various animal models used to investigate the impact of prenatal and postnatal injury (hypoxic, ischemic or combinatory) on living organisms, and show their advantages and limitations.
- MeSH
- Humans MeSH
- Inflammation Mediators metabolism MeSH
- Brain growth & development metabolism MeSH
- Hypoxia, Brain metabolism pathology MeSH
- Animals, Newborn MeSH
- Infant, Newborn MeSH
- Oxidative Stress physiology MeSH
- Receptors, N-Methyl-D-Aspartate metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Infant, Newborn MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Inflammation Mediators MeSH
- Receptors, N-Methyl-D-Aspartate MeSH