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We previously found that Lewis (LEW/N) hypothalamic cells respond to interleukin-1beta (IL-1beta) with reduced corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) peptide synthesis and secretion compared to Fischer (F344/N) cells. To investigate whether this peptide hyporesponsiveness in LEW/N cells is secondary to their deficient mRNA(More)
Endogenous hypothalamic pro-inflammatory cytokines modulate the hypothalamic-pituitary-adrenal (HPA) axis responses. To investigate whether hypothalamic IL-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha) are associated with differential inflammatory susceptibilities between Lewis (LEW/N) and Fischer (F344/N) rats, mRNA levels of pro-inflammatory(More)
Lewis (LEW/N) rats, compared to Fischer (F344/N) rats, are susceptible to inflammatory/autoimmune diseases, in part, as a result of their blunted hypothalamic-pituitary-adrenal (HPA) axis responses. We examined regulation of LEW/N and F344/N fetal hypothalamic cell secretion of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), two major(More)
By producing brain-derived neurotrophic factor (BDNF), astrocytes play a role in disease resistance. This study was undertaken to investigate whether primary astrocytes derived from LEW/N and F344/N rats differentially express BDNF. LEW/N astrocytes expressed more BDNF mRNA and protein than F344/N astrocytes in basal and valproic acid (VPA)-stimulated(More)
The aim of this study is to test whether inflammatory responsiveness of rat microglial cells is strain-specific in primary microglia derived from neonatal LEW/N and F344/N rats. In contrast to F344/N microglia, LEW/N microglia constitutively and upon lipopolysaccharide challenge expressed higher levels of mRNA for the majority of inflammatory mediators(More)
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