Brain nuclear factor kappa B is involved in the corticotropin-releasing factor-induced central activation of sympatho-adrenomedullary outflow in rats.

Abstract:

:Using urethane-anesthetized rats, we examined whether an activation of nuclear factor kappa B is involved in the corticotropin-releasing factor-induced increase in plasma levels of catecholamines. An intracerebroventricularly administered corticotropin-releasing factor (1.5 nmol/animal)-induced increase of plasma catecholamines was dose-dependently reduced by pyrrolidine dithiocarbamate (a nuclear factor kappa B antagonist) (1 and 9 nmol/animal, intracerebroventricularly) and SN50 (a peptide inhibiting nuclear factor kappa B translocation) (9 and 18 nmol/animal, intracerebroventricularly), while SN50M (an inactive control peptide for SN50, 19 nmol/animal, intracerebroventricularly) had no effect on the corticotropin-releasing factor-induced elevation of both catecholamines. Furthermore, the corticotropin-releasing factor-induced responses were also attenuated by rosiglitazone (a peroxisome proliferator-activated receptor-gamma agonist)(50 nmol/animal, intracerebroventricularly). These results suggest the involvement of brain nuclear factor kappa B in the corticotropin-releasing factor-induced central activation of the sympatho-adrenomedullary outflow in rats.

journal_name

Eur J Pharmacol

authors

Okada S,Yamaguchi-Shima N,Shimizu T,Arai J,Yorimitsu M,Yokotani K

doi

10.1016/j.ejphar.2008.01.037

subject

Has Abstract

pub_date

2008-04-14 00:00:00

pages

207-12

issue

1

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(08)00111-8

journal_volume

584

pub_type

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