Philos Trans R Soc Lond B Biol Sci
May 2015
The evolution of the field of neuroscience has been propelled by the advent of novel technological capabilities, and the pace at which these capabilities are being developed has accelerated dramatically in the past decade. Capitalizing on this momentum, the United States launched the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative to develop and apply new tools and technologies for revolutionizing our understanding of the brain. In this article, we review the scientific vision for this initiative set forth by the National Institutes of Health and discuss its implications for the future of neuroscience research.
View Article and Find Full Text PDFLate fetal and early postnatal iron deficiency (ID) is a common condition that causes learning and memory impairments in humans while they are iron deficient and following iron repletion. Rodent models of fetal ID demonstrate significant short- and long-term hippocampal structural and biochemical abnormalities that may predispose hippocampal area CA1 to abnormal electrophysiology. Rat pups made iron deficient during the fetal and early postnatal period were assessed for basal synaptic transmission, paired-pulse facilitation (PPF), and long-term potentiation (LTP) in CA1 at postnatal days (P)15 and P30 while iron deficient and at P65 following iron repletion.
View Article and Find Full Text PDFIron deficiency early in life is associated with cognitive disturbances that persist beyond the period of iron deficiency. Within cognitive processing circuitry, the hippocampus is particularly susceptible to insults during the perinatal period. During the hippocampal growth spurt, which is predominantly postnatal in rodents, iron transport proteins and their messenger RNA stabilizing proteins are upregulated, suggesting an increased demand for iron import during this developmental period.
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