Hypothalamus, anterior pituitary and adrenal gland involvement in the activation of adrenocorticotropin and corticosterone secretion by gastrin-releasing peptide

The role of gastrin-releasing peptide on conditioned fear: differential cortical and amygdaloid responses in the rat

“…Furthermore, it modulates the expression of corticotropin releasing hormone (CRH) at stress-relevant brain sites, including the central nucleus of the amygdala (CeA) (Kent et al 2001a). The administration of GRP to in vitro cell cultures of the hypothalamus, the pituitary, or the adrenal cortex provoked the release of CRH, adrenocorticotropic hormone (ACTH) and corticosterone, respectively (Garrido et al 1999). In rodents, as well, pretreatment with GRP receptor antagonists attenuated serotonin release at the hypothalamus under both basal and restraint stressor conditions (Garrido et al 2002).…”

Sexually diergic, dose-dependent hypothalamic–pituitary–adrenal axis responses to nicotine in a dynamic in vitro perfusion system

“…Each hypothalamic and pituitary tissue-half and each adrenal gland was weighed and placed individually in beakers containing modified Bradbury tissue culture medium (pH 7.4) at 37°C (Bradbury et al, 1974; Garrido et al, 1999). The culture medium contained (in mM) 126 NaCl, 6 KCl, 0.88 MgSO 4 , 1 Na 2 HPO 4 , 22 NaHCO 3 , 1.45 CaCl 2 , 11 glucose, and 0.05 ascorbic acid (all reagents from Sigma, St. Louis, MO, USA).…”

Gastrin-releasing peptide links stressor to cancer progression

“…The competitive and speciWc GRP receptor antagonist (Leu13--CH2NH-Leu14) had no eVect on the basal secretion of corticotropin-releasing factor (CRF)-like material, ACTH, and corticosterone; however, it (100 nM) completely blocked the stimulatory eVects of GRP on bioactive releases of CRF, ACTH, and corticosterone (Garrido et al 1998(Garrido et al , 1999Shimizu et al 2005). It indicated that GRP enhanced stress response by activation of both SNS and HPA, because ganglionic blockade or adrenalectomy abolished the GRPinduced increase of plasma EPI concentration, and antagonism of GRP action attenuated the behavioral and neurochemical eVects of stressors (Brown and Fisher 1984;Okubo et al 1985;Garrido et al 1998Garrido et al , 1999Gonzalez et al 2008). Although the mechanism of GRP in regulation of stress response is not fully understood so far, the current data strongly suggest that GRP plays a pivotal role in mediating the eVects of stress and may inXuence cancer growth and metastasis through stress hormones and GCs (Fig.…”