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首页> 外文期刊>International journal of developmental neuroscience: the official journal of the International Society for Developmental Neuroscience >Undernourishment and recurrent seizures early in life impair Long-Term Potentiation and alter NMDAR and AMPAR expression in rat hippocampus
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Undernourishment and recurrent seizures early in life impair Long-Term Potentiation and alter NMDAR and AMPAR expression in rat hippocampus

机译：生命早期的营养不良和复发性癫痫发作损害了长期的增强，并改变了大鼠海马的NMDAR和AMPAR表达

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Undernourishment is a global issue, especially in developing countries, affecting newborns and children in a vulnerable period of brain development. Previous studies of undernourishment models suggested a relationship between undernourishment and epilepsy. The exposure to both undernourishment and recurrent seizures early in life appears to have detrimental effects on the developing brain. This study aims to investigate the neurobiological consequences of undernourishment and recurrent seizures exposure early in life, investigating Long Term Potentiation (LTP) induction and gene expression of NMDA receptor subunits in the hippocampus during adulthood (P60). Animals were exposed to maternal deprivation protocol from P2 to P15 to control food intake in rat pups and Flurothyl-induced seizures from P7 to P10. Electrophysiological records of hippocampal slices were recorded and gene expression of NR1A, NR2A, NR2B, NR2C, NR2D and BDNF were investigated. Animals exposed to undernourishment or recurrent seizures failed to promote LTP after stimulation. Furthermore, seizure exposure early in life led to increased expression of hippocampal NR1A, NR2A, NR2B, NR2C and NR2D when compared to controls. Interestingly, when animals were exposed to undernourishment paradigm early in life, this upregulation of NDMA subunits was absent. In conclusion, our study showed impaired LTP after undernourishment and recurrent seizures early in life, together with differential expression of NDMA expression in the hippocampus during adulthood.
机译：营养不良是一个全球性问题，特别是在发展中国家，影响新生儿和弱势脑发展时期的儿童。以前对营养不良模型的研究表明营养不良和癫痫之间的关系。在生命中早期接触营养不良和复发性癫痫发作似乎对显影大脑产生了不利影响。本研究旨在探讨生命早期营养不良和复发性癫痫发育的神经生物学后果，研究了在成年期间海马在海马中的长期增强（LTP）诱导和基因表达。将动物从P2到P15暴露于母体剥夺方案，以控制大鼠幼崽的食物摄入量和从P7到P10的血管诱导的癫痫发作。研究了海马切片的电生理记录，研究了NR1A，NR2A，NR2B，NR2C，NR2D和BDNF的基因表达。暴露于营养不良或复发性癫痫发作的动物未能在刺激后促进LTP。此外，与对照相比，癫痫发育率在生命期间早期导致海马NR1A，NR2A，NR2B，NR2C和NR2D的表达增加。有趣的是，当动物早期暴露在生命期间暴露于营养不良的范式时，缺乏这种NDMA亚基的上调。总之，我们的研究表明，在生命期间的营养不良和复发性癫痫发作后，患有损害的LTP，以及在成年期间海马中NDMA表达的差异表达。

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