Basal and IL-1β-stimulated cytokine and neuropeptide mRNA expression in brain regions of young and old Long–Evans rats

Abstract

Listen

Translate article

Young and old Long–Evans rats respond with fevers of equal magnitude and duration to the brain administration of interleukin-1β (IL-1β). Here, we characterized brain regional mRNA expression of cytokine and neuropeptide components in response to the brain administration of IL-1β. We used specific and highly sensitive RNase protection assays to determine mRNA changes for IL-1β, IL-1 receptor type I (IL-1RI), IL-1R accessory proteins I and II (IL-1R AcP I and II), IL-1 receptor antagonist (IL-1Ra), transforming growth factor-β1 (TGF-β1), glycoprotein 130 (gp 130), leptin receptor (OB-R), neuropeptide Y (NPY) and pro-opiomelanocortin (POMC) in the cerebellum, parieto-frontal cortex, hippocampus, hypothalamus, and midbrain of male young (3–5 months) and old (24–26 months) Long–Evans rats. In both young and old rats, IL-1β induced a significant up-regulation of cerebellar IL-1Ra, IL-1RI, and TGF-β1 mRNAs; hippocampal TGF-β1 mRNA; hypothalamic IL-1β, IL-1Ra, TGF-β1, and gp 130 mRNAs; and midbrain IL-1β and TGF-β1 mRNAs. There were no age-related differences in any cytokine mRNA levels under basal or IL-1β-stimulated conditions. Levels of hypothalamic POMC mRNA were different between age groups under basal and stimulated conditions. IL-1R AcP I and leptin receptor did not change in any brain region from either young or old rats, suggesting specificity of transcriptional changes. The data show that old Long–Evans rats are not defective in their capacity to develop an appropriate cytokine response to the brain administration of IL-1β. The implications of these findings for neuroimmunological–neuroinflammatory and neurotoxic/neurodegenerative processes are discussed.