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Chronic Pain Induced Inflammation in the Hypothalamus of Rats
Author(s) -
DeForest Elizabeth,
Semke Lori,
Duric Vanja,
Clayton Sarah C
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.lb466
Subject(s) - medicine , hypothalamus , inflammation , endocrinology , chronic pain , central nervous system , sympathetic nervous system , blood pressure , psychiatry
Chronic pain has been shown in humans to be associated with cardiovascular disease and hypertension but the mechanism of that association is unclear. Our overall hypothesis of this study is that chronic pain has a sensitizing effect on the central nervous system (CNS) that increases sympathetic nerve activity and predisposes to hypertension. Because inflammation can influence neuronal activation, in this study, we hypothesized that chronic pain generates a pro‐inflammatory phenotype in the cardiovascular control centers in the brain (e.g. the paraventricular nucleus of the hypothalamus). A chronic inflammatory pain model was generated by CFA injection into the left hind paw. Animals were then sacrificed 24 hours after the injection (acute phase) or 14 days following the injection (Chronic phase). RNA was isolated from the samples and expression of the pro‐ and anti‐inflammatory markers were assessed by RT‐qPCR. The expression of the pro‐inflammatory marker interleukin ‐ 1β (IL‐1β) was elevated in the hypothalamus 24 hours after CFA injection (2.3‐fold vs sham) and remained elevated at 14 days (2.5‐fold vs. sham) (P= .002). The expression of an anti‐inflammatory marker, transforming growth factor‐β 1 (TGF‐β 1), was decreased in the hypothalamus 24 hours after CFA injection (.8‐fold vs. sham) and remained decrease at 14 days (.63‐fold vs. sham) (P=.05) This data suggests that chronic pain induces a rapid and sustained pro‐inflammatory phenotype in the hypothalamus. This could lead to inappropriate activation of the sympathetic nervous system that could contribute to the development of hypertension. Support or Funding Information SC IOER This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .