Fujimoto Naohiro
   Department   School of Medicine  Urology, Clinical Medical Sciences
   Position  
Article types journal article
Language English
Peer review Non peer reviewed
Title Upregulation of corticotropin-releasing hormone gene expression in the paraventricular nucleus of cyclophosphamide-induced cystitis in male rats.
Journal Formal name:Brain research
Abbreviation:Brain Res
ISSN code:00068993/00068993
Domestic / ForeginForegin
Volume, Issue, Page 1018(2),193-200頁
Author and coauthor Mineta Kaori, Nomura Masayoshi, Terado Michikazu, Fujimoto Naohiro, Sasaguri Takakazu, Ueta Yoichi, Matsumoto Tetsuro
Publication date 2004/08
Summary We examined the effects of cyclophosphamide (CP)-induced cystitis on the expression of corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus (PVN) and the serum levels of adrenocorticotropic hormone (ACTH) using in situ hybridization histochemistry and radioimmunoassay. In addition, the expression of AVP heteronuclear (hn) RNA and neuronal nitric oxide synthase (nNOS) mRNA was also examined in the PVN of a CP-induced cystitis model. We found that the levels of CRH mRNA were significantly increased in the PVN at 2 h after intraperitoneal administration of CP compared to those in saline-treated rats. The CRH mRNA levels in the PVN peaked at 12 h after CP administration and the levels were still significantly higher than those in saline-treated group at 24 h after CP administration. The serum ACTH levels in CP-treated group were also significantly higher compared to those in saline-treated group at any of the time points examined. Unlike previous findings showing upregulation of nNOS mRNA and AVP hnRNA under somatic nociceptive states, the levels of nNOS mRNA and AVP hnRNA were unchanged in the PVN following CP-induced cystitis, visceral nociceptive stimulation. These results suggest that visceral nociceptive stimulation as well as somatic nociceptive stimulation may activate the hypothalamo-pituitary axis but the hypothalamic neuroendocrine responses produced by visceral nociceptive stimulation may be different from those produced by somatic nociceptive stimulation.
DOI 10.1016/j.brainres.2004.05.063
PMID 15276878