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https://doi.org/10.1016/S0891-5849(97)00367-5 Yang , Joy C. ; Cortopassi , Gino A. / Induction of the mitochondrial permeability transitioncausesrelease of the apoptogenic factor
Bradykinin , acetylcholine , adrenalin , and prostaglandin(passive) is triggered byThe release of releasing factor
the stress responsecausesthe release of corticotropin - releasing factor
the NAD+ dependent protein deacetylase sirtuin-6 and nuclear factor kappa B sequester GR expressionleadingto disinhibition of corticotropin releasing factor
CRF(1)-R activation of the dynorphin / kappa opioid receptor ( KOR ) system(passive) were triggered byCorticotropin Releasing Factor ( CRF
prolonged sittingcausesthe release of corticotropin - releasing factor
However , in most cases , Rb function is lost because of phosphorylation by the CDKsleadingto release of the transcriptional factor
CRF ) family of neuropeptides(passive) is composedThe corticotropin - releasing factor
IIR(passive) caused byproinflammatory factor release
from stressresultingfrom stress
to the production of adrenocorticotropin , which causes adrenal secretion of cortisolleadsto the production of adrenocorticotropin , which causes adrenal secretion of cortisol
in increased cortisol secretion from the adrenal gland ( 4resultingin increased cortisol secretion from the adrenal gland ( 4
the pituitary to release ACTHcausesthe pituitary to release ACTH
the release of dynorphin , the endogenous ligand for kappa opioid receptors ... in limbic brain regions including the basolateral amygdala ( BLA ) and dorsal raphe nucleus ( DRN ) to produce a negative affective statecausesthe release of dynorphin , the endogenous ligand for kappa opioid receptors ... in limbic brain regions including the basolateral amygdala ( BLA ) and dorsal raphe nucleus ( DRN ) to produce a negative affective state
ACTH hypersecretion and hypercortisolismcausesACTH hypersecretion and hypercortisolism
a sudden burst of dehydroepiandrosterone ( DHEA(passive) caused bya sudden burst of dehydroepiandrosterone ( DHEA
an increase in cortisol levels and enhanced severity of insulin resistance in the hippocampus.6,28causesan increase in cortisol levels and enhanced severity of insulin resistance in the hippocampus.6,28
the plasma levels of somatostatin , gastrin or cholecystokinin when administered intracerebroventricularly to ratsinfluencesthe plasma levels of somatostatin , gastrin or cholecystokinin when administered intracerebroventricularly to rats
to an increase in neuronal activity ... stimulating the production of Aβ , and demonstrating a link between depression and AD development ( Dong and Csernansky , 2009leadsto an increase in neuronal activity ... stimulating the production of Aβ , and demonstrating a link between depression and AD development ( Dong and Csernansky , 2009
type-2 receptor and corticotropin - releasing factor - binding protein coexist in rat ventral tegmental area nerve terminalsoriginatedtype-2 receptor and corticotropin - releasing factor - binding protein coexist in rat ventral tegmental area nerve terminals
a cascade of eventscausesa cascade of events
relaxation of the uterine artery in a concentration - dependent manner and the relaxation was decreased at term compared with late pregnancy ( p < 0.05causedrelaxation of the uterine artery in a concentration - dependent manner and the relaxation was decreased at term compared with late pregnancy ( p < 0.05
prepulse inhibition(passive) caused byprepulse inhibition
gastric motor function(passive) triggered bygastric motor function
down - to - up state transitions [ 41can triggerdown - to - up state transitions [ 41
in an allostatic modelresultingin an allostatic model
Dr. Berridge saidcreatesDr. Berridge said