Glucocorticoid Fast Feedback Inhibition of Stress-Induced ACTH Secretion in the Male Rat: Rate Independence and Stress-State Resistance

Autor: Ryan J. Newsom, Mariana Rodriguez-Santiago, Elizabeth R. Woodruff, Chad D. Osterlund, Robert L. Spencer, Anjali P. Chadayammuri
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Restraint
Physical

medicine.medical_specialty
endocrine system
Hypothalamo-Hypophyseal System
Corticotropin-Releasing Hormone
medicine.medical_treatment
Pituitary-Adrenal System
Adrenocorticotropic hormone
Biology
Rats
Sprague-Dawley

03 medical and health sciences
Corticotropin-releasing hormone
chemistry.chemical_compound
0302 clinical medicine
Endocrinology
Adrenocorticotropic Hormone
Corticosterone
Stress
Physiological

Negative feedback
Internal medicine
medicine
polycyclic compounds
Animals
Original Research
Feedback
Physiological

Adrenalectomy
Rats
030104 developmental biology
Glucocorticoid secretion
chemistry
030217 neurology & neurosurgery
Glucocorticoid
hormones
hormone substitutes
and hormone antagonists

Stress
Psychological

medicine.drug
Hormone
Paraventricular Hypothalamic Nucleus
Popis: Normal glucocorticoid secretion is critical for physiological and mental health. Glucocorticoid secretion is dynamically regulated by glucocorticoid-negative feedback; however, the mechanisms of that feedback process are poorly understood. We assessed the temporal characteristics of glucocorticoid-negative feedback in vivo using a procedure for drug infusions and serial blood collection in unanesthetized rats that produced a minimal disruption of basal ACTH plasma levels. We compared the negative feedback effectiveness present when stress onset coincides with corticosterone's (CORT) rapidly rising phase (30 sec pretreatment), high plateau phase (15 min pretreatment), or restored basal phase (60 min pretreatment) as well as effectiveness when CORT infusion occurs after the onset of stress (5 min poststress onset). CORT treatment prior to stress onset acted remarkably fast (within 30 sec) to suppress stress-induced ACTH secretion. Furthermore, fast feedback induction did not require rapid increases in CORT at the time of stress onset (hormone rate independent), and those feedback actions were relatively long lasting (≥15 min). In contrast, CORT elevation after stress onset produced limited and delayed ACTH suppression (stress state resistance). There was a parallel stress-state resistance for CORT inhibition of stress-induced Crh heteronuclear RNA in the paraventricular nucleus but not Pomc heteronuclear RNA in the anterior pituitary. CORT treatment did not suppress stress-induced prolactin secretion, suggesting that CORT feedback is restricted to the control of hypothalamic-pituitary-adrenal axis elements of a stress response. These temporal, stress-state, and system-level features of in vivo CORT feedback provide an important physiological context for ex vivo studies of molecular and cellular mechanisms of CORT-negative feedback.
Databáze: OpenAIRE
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