title: Effect of glucocorticoids on the adrenocortical axis responses to electrical stimulation of the amygdala and the ventral noradrenergic bundle.
abstract: In the present study we examined the negative feedback effect of exogenous and endogenous glucocorticoids (GC) on the responses of the hypothalamo-pituitary-adrenocortical (HPA) axis to electrical stimulation of the central amygdaloid nucleus (AMG) and the ventral noradrenergic bundle (VNAB). Injection of dexamethasone (DEX 5-50 microg/kg BW) 3.5 h prior to the electrical stimuli inhibited the serum ACTH and corticosterone (CS) responses in a dose dependent manner. At a dose of 50 microg/kg BW DEX, the stress induced responses was completely abolished. Pretreatment with a subcutaneous injection of corticosteroid type II receptor antagonist (RU-38486) 30 mg/kg BW, enhanced the ACTH and CS responses to both stimuli. In contrast, the type I receptor antagonist (RU-28381) did not affect neither the responses to both stimuli nor the inhibitory effect exerted by DEX. Electrical stimulation of both the AMG and VNAB caused a significant depletion of CRF-41 content of the median eminence (ME). Pretreatment with DEX (50 microg/kg BW) inhibited the electrical stimuli-induced depletion of ME CRH-41. These results suggest that: (1) the HPA axis responses to electrical stimuli of the AMG and the VNAB are sensitive to the negative feedback of GC; (2) the feedback effect exerted by GC is mediated by type II GC receptors; (3) CRH-41 released from the ME plays a dynamic role in mediating pituitary-adrenocortical responses to the electrical stimuli; (4) the inhibitory effect of exogenous DEX is mediated by a reduction of CRF-41 release from the ME.
authors.affiliation: Department of Neurology, Hadassah University Hospital, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
authors.forename: J
authors.initials: J
authors.lastname: Weidenfeld
authors.forename: A
authors.initials: A
authors.lastname: Itzik
authors.forename: S
authors.initials: S
authors.lastname: Feldman
mesh_terms: D000302:Adrenal Cortex / Q000502:physiology; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism; D000679:Amygdala / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D003345:Corticosterone / Q000097:blood / Q000378:metabolism; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D004558:Electric Stimulation; D005246:Feedback; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000502:physiology*; D008297:Male; D015735:Mifepristone / Q000494:pharmacology; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D013148:Spironolactone / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000451:Mineralocorticoid Receptor Antagonists; D013148:Spironolactone; D015735:Mifepristone; C041006:RU 28318; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone