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- W2000401108 abstract "Pro-inflammatory cytokines, especially Interleukin (IL)-6, are elevated in the brains and serum of very premature infants in association with perinatal infectious and hypoxic/ischemic insults. To determine potential adverse effects of IL-6 on brain development, cross-fostered litters of male cd-1 mice were injected subcranially with hyper-IL-6 or vehicle at postnatal day (pnd) 4 and examined for alterations in functional landmarks of CNS development. No acute injury response was evident at 1–7 days following hyper-IL-6 injection as determined by glial morphology and RNase protection assays for acute response genes, ICAM-1, iNOS, Mac-1, A-20, and EB-22. In preweanling mice, reflex ontogeny and physical markers of development were not altered; however, exposed mice demonstrated increased over-generalized motor responses (Fox Battery) leading to an overall impression of hyper-reactivity and hyperactivity. At pnd 24 and 80, assessment of autonomic, sensory, and motor systems (Functional Observation Battery) showed persistence of hyper-reactivity and hyperactivity. Learning and memory were assessed by passive avoidance (PA) at pnd 24 and by radial arm maze (RAM) in adults. Hyper-IL-6 exposure significantly impaired PA performance. RAM performance was similar between hyper-IL-6 and control groups in acquisition of win-shift task but hyper-IL-6 animals showed deficits on repeated acquisition task. The persistent hyperactive, hyper-reactive behavioral phenotype evident in hyper-IL-6 exposed mice appeared to interfere with performance on both learning and memory tasks, suggesting that early exposure of the developing brain to IL-6 can have persistent adverse functional effects and raising additional concerns for effects of immune mediators in premature infants." @default.
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- W2000401108 date "2008-06-28" @default.
- W2000401108 modified "2023-09-27" @default.
- W2000401108 title "Poster Sessions CP03: Trophic Factors" @default.
- W2000401108 doi "https://doi.org/10.1046/j.1471-4159.81.s1.32_1.x" @default.
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