| Literature DB >> 26416672 |
Silvia Honda Takada1, Lívia Clemente Motta-Teixeira2, Aline Vilar Machado-Nils2, Vitor Yonamine Lee3, Carlos Alberto Sampaio3, Roberson Saraiva Polli4, Jackeline Moraes Malheiros4, Luiz Fernando Takase5, Alexandre Hiroaki Kihara6, Luciene Covolan4, Gilberto Fernando Xavier2, Maria Inês Nogueira3.
Abstract
Neonates that suffer oxygen deprivation during birth can have long lasting cognitive deficits, such as memory and learning impairments. Hippocampus, one of the main structures that participate in memory and learning processes, is a plastic and dynamic structure that conserves during life span the property of generating new cells which can become neurons, the so-called neurogenesis. The present study investigated whether a model of rat neonatal anoxia, that causes only respiratory distress, is able to alter the hippocampal volume, the neurogenesis rate and has functional implications in adult life. MRI analysis revealed significant hippocampal volume decrease in adult rats who had experienced neonatal anoxia compared to control animals for rostral, caudal and total hippocampus. In addition, these animals also had 55.7% decrease of double-labelled cells to BrdU and NeuN, reflecting a decrease in neurogenesis rate. Finally, behavioral analysis indicated that neonatal anoxia resulted in disruption of spatial working memory, similar to human condition, accompanied by an anxiogenic effect. The observed behavioral alterations caused by oxygen deprivation at birth might represent an outcome of the decreased hippocampal neurogenesis and volume, evidenced by immunohistochemistry and MRI analysis. Therefore, based on current findings we propose this model as suitable to explore new therapeutic approaches.Entities:
Keywords: Anxiety; Hippocampal neurogenesis; MRI; Neonatal anoxia; Working memory
Mesh:
Year: 2015 PMID: 26416672 DOI: 10.1016/j.bbr.2015.08.039
Source DB: PubMed Journal: Behav Brain Res ISSN: 0166-4328 Impact factor: 3.332