Ucp2 Induction by Natural Birth and Hippocampus Development

Ucp2 Induction by Natural Birth and Hippocampus Development

A recent report published in the August issue of PLoS One indicates that natural (vaginal) birth but not Caesarian section birth in mice triggers uncoupling protein 2 (Ucp2) expression in hippocampal neurons.

Mitochondrial Ucp2 is a critical determinant of fatty acid utilization by adult neurons and is involved in cell proliferation, neuroprotection and synaptogenesis in the adult brain.

In the PLoS One study, Julia Simon-Areces and colleagues from the Cajal institute in Spain; the Federal University of Rio Grande do Sul, Brazil, and the Yale University School of Medicine, US investigated the Ucp2 induction in the hippocampus perinatally, and the Ucp2-associated cellular mechanisms involved in the development of neuronal circuits in vitro with implications for adult behavior.

Ucp2 mRNA levels were induced in newborns by vaginal birth, and significantly higher level of Ucp2 protein expression was observed at the day of delivery in animals that were born via vaginal birth compared to those with Cesarean section.

In naturally born mice, Ucp2 protein remained elevated early postnatally, as well as in adulthood. According to the authors, their findings are consistent with previous reports indicating beneficial effects of Ucp2 and high fat content of breast milk, related to protection of febrile seizures in early postnatal animals. The authors suggest that Ucp2 mRNA induction may be associated with hypoxia/ischemia that accompanies vaginal birth.

In many countries Caesarian sections are performed in more than 30% of all births. This report is probably among the first to address and study in details, in experimental conditions, a possible relationship between natural birth and brain development.

SOURCE: PLoS One, 2012, 7(8):e42911. Epub 2012 Aug 8

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Source: Cover Image: Laszlo Seress' preparation of a human hippocampus alongside a sea horse. Author: Professor Laszlo Seress. Credit: Wikimedia Commons.

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