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Submitted on November 1, 2004
Accepted on December 6, 2004
Tupper Research Institute and Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Tufts-New England Medical Center, Boston, MA 02111. Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest H-1083 Hungary. Department of Community Health, Tufts University School of Medicine, Boston, MA 02111. Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111
* To whom correspondence should be addressed. E-mail: rlechan{at}tufts-nemc.org.
The nonthyroidal illness syndrome associated with fasting, infection and chronic illness, is characterized by low thyroid hormone levels and low or inappropriately normal thyroid-stimulating hormone (TSH) levels in the circulating blood, and reduced synthesis of TSH-releasing hormone (TRH) in hypophysiotropic neurons residing in the hypothalamic paraventricular nucleus (PVN). To test the hypothesis that ascending brain stem pathways are involved in mediation of bacterial lipopolysaccharide (LPS)-induced suppression of TRH mRNA in the PVN, we unilaterally transected brain stem pathways to the PVN and determined the effects of LPS on TRH gene expression, and as a control, on CRH gene expression in hypophysiotropic neurons using semiquantitative in situ hybridization histochemistry. Efficacy of the transection was determined by immunocytochemical detection of ascending adrenergic pathways in the PVN. In vehicle treated animals, CRH mRNA in the PVN showed significant reduction on the transected side compared with intact side, whereas a significant increase in TRH mRNA was observed on the transected side compared with intact side. Following LPS administration (250 µg/100 g BW), a dramatic increase in CRH mRNA was observed on the intact side and a significantly less increase on the transected side. In contrast, LPS treatment resulted in reduction in TRH mRNA on the transected side compared with the intact side, and a significant reduction in TRH mRNA on the transected side compared with vehicle treated animals. These studies confirm an important role of ascending brain stem projections in LPS-induced activation of CRH gene expression, but indicate that they do not mediate the effect of LPS to inhibit hypophysiotropic TRH gene expression.
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