We demonstrate for the first time that mifepristone, a wellestablished
antagonist of GR, also knocks down GR protein expression
in rainbow trout. This led to an attenuation in stressor-induced
plasma cortisol level suggesting that both central and
peripheral GR signaling may be involved in HPI axis functioning.
Specifically, we provide evidence that GR signaling is required for
maintaining basal CRF and StAR transcript levels in the POA and
head kidney, respectively, both of which are critical components
of the endocrine stress response. A similar study that incorporates
a more severe and/or chronic stressor is needed to fully elucidate
the impact of GR knockdown and antagonism on the endocrine
stress axis. Overall GR signaling is essential for the functioning of
HPI axis and resultant elevation of plasma cortisol levels, a highly
conserved response to stress in vertebrates, and any impact on this
receptor function may lead to diminished stress performance.