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

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-γ 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.