Impact of perinatal hypoxia on the developing brain

Title:

Impact of perinatal hypoxia on the developing brain

Creator:

Piešová, Michaela and Mach, Mojmír

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:a1242c2e-97f2-4b7e-bb90-2e099ea32254
uuid:a1242c2e-97f2-4b7e-bb90-2e099ea32254
doi:10.33549/physiolres.934198

Subject:

excitotoxicity, ROS, hypoxic model, emotionality, and cognition

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

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.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

199-213

Source:

Physiological research | 2020 Volume:69 | Number:2

Harvested from:

CDK

Metadata only:

false