Effects of oxygen deprivation in the central nervous system of neonates

• Processo: 14/12116-6
• Modalidade de apoio: Auxílio Organização - Reunião Científica
• Data de Início da vigência: 08 de setembro de 2014
• Data de Término da vigência: 21 de setembro de 2014
• Área do conhecimento: Interdisciplinar
• Pesquisador responsável: Maria Inês Nogueira
• Beneficiário: Maria Inês Nogueira
• Instituição Sede: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brasil
• Assunto(s): Hipóxia Morte celular Neurociências
• Palavra(s)-Chave do Pesquisador: anoxia | cell death | hipóxia-isquemia | hypoxia neonatal | interaction mother - child | Neonatal oxygen deprivation | neurodegeneration | Neurociencias

Resumo

EFFECTS OF OXYGEN DEPRIVATION IN THE CENTRAL NERVOUS SYSTEM OF NEONATES, comprise 4 lectures: 1.Neonatal Anóxia a worldwide clinical problem requiring Research and Science Public understanding2.Effects Of Oxygen Deprivation In The Central Nervous System Of Neonates3.Role of innate immune receptors in a model of perinatal brain injury4.Neuroimaging to Uncover Secrets of Cerebral PalsyThe first analyses the causes and consequences of the oxygen deprivation at the neonatal period which may alter the somatic, neural and behavioral body´s development, according to the time of its onset and the age of the child at that moment. Some of them might represent long lasting deficts. Statistics report neonatal anoxia as a major cause of brain injury at birth. It affects 0.1 to 0.3% of full-term infants, and approximately 60% of low-weight premature infants, thus constituting a major public health concern. Then, the cellular and subcellular patterns of hippocampal neuronal cell death following anoxia model in neonatal rats, by combining different techniques such as TUNEL (DNA fragmentation), Fluoro-Jade® B (FJB), cleaved caspase-3 immunohistochemistry (IHC) and transmission electron microscopy, are presented and discussed. The third lecture, investigates the impairments in newborns and how neuroinflammation contributes to the long-term outcome after a perinatal brain injury with the fractalkine receptor chemokine CX3C motif receptor 1 (CX3CR1) and of toll-like receptor (TLR) signaling. The fourth lecture, analises the dogma that neurodevelopmental deficits, including cerebral palsy (CP), are caused by preventable events at birth. But, as the timing of the insult in the antenatal and natal period is unknown, it is suggested that fetal neuroimaging may be useful for discovering important insults that have long-term consequences using a rabbit model of cerebral palsy. (AU)