Hypothalamic Control of Adrenocorticotropin Secretion: Advances since the Discovery of 41-Residue Corticotropin-Releasing Factor

Antoni, Ferenc András

doi:10.1210/edrv-7-4-351

Cited by 923 publications

(443 citation statements)

References 110 publications

(217 reference statements)

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“…Adrenocorticotropic hormone then travels through the bloodstream and initiates glucocorticoid release from the adrenal cortex (Vale et al, 1981;Antoni, 1986;Owens and Nemeroff, 1991). Glucocorticoids (ie, cortisol in humans, corticosterone in rodents; CORT) aid in energy mobilization and help to restore homeostasis via negative feedback mechanisms after a threat has passed (Munck et al, 1984;Sapolsky et al, 2000).…”

Section: Stress Responsementioning

confidence: 99%

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Perusini

Meyer

Long

et al. 2015

Neuropsychopharmacol

100

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Fear promotes adaptive responses to threats. However, when the level of fear is not proportional to the level of threat, maladaptive fear-related behaviors characteristic of anxiety disorders result. Post-traumatic stress disorder develops in response to a traumatic event, and patients often show sensitized reactions to mild stressors associated with the trauma. Stress-enhanced fear learning (SEFL) is a rodent model of this sensitized responding, in which exposure to a 15-shock stressor nonassociatively enhances subsequent fear conditioning training with only a single trial. We examined the role of corticosterone (CORT) in SEFL. Administration of the CORT synthesis blocker metyrapone prior to the stressor, but not at time points after, attenuated SEFL. Moreover, CORT co-administered with metyrapone rescued SEFL. However, CORT alone without the stressor was not sufficient to produce SEFL. In these same animals, we then looked for correlates of SEFL in terms of changes in excitatory receptor expression. Western blot analysis of the basolateral amygdala (BLA) revealed an increase in the GluA1 AMPA receptor subunit that correlated with SEFL. Thus, CORT is permissive to trauma-induced changes in BLA function.

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Section: Stress Responsementioning

confidence: 99%

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Perusini

Meyer

Long

et al. 2015

Neuropsychopharmacol

100

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“…Indeed, there is scant information as to the nature of adrenocorticotrophin (ACTH) and cortisol secretion during this important stage of foetal development. In adult animals, ACTH m d cortisol secretion is pulsatile (2) and a complex interaction between a number of neurotransmitter and neuropeptide systems, regulate the activity of this axis (3). However, until recently, few of these systems have received attention with respect to the development of neuroendocrine control in the foetus.…”

mentioning

confidence: 99%

Effects of Naloxone on the Preparturient Increase in Adrenocorticotrophin and Cortisol in Foetal Sheep

Challis

1991

J Neuroendocrinology

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Parturition in sheep is preceded by a rapid increase in foetal pituitary-adrenal activity. Administration of exogenous opioids increases foetal plasma adrenocorticotrophin (ACTH) and cortisol concentrations after Day 125 of pregnancy (term = 145 days). In order to test the hypothesis that endogenous opioids regulate the increase in pituitary-adrenal activity prior to parturition in foetal sheep, we measured changes in plasma ACTH and cortisol in response to administration of either naloxone (1.2 mg intravenous bolus followed by a 2.5 mg/h continuous infusion for 2 h; foetal body weight approximately 2.5 kg) or saline to chronically catheterized foetal sheep at 2-day intervals between Day 140 and the onset of parturition. In addition, we utilized a computerized algorithm (Munro) to examine the precise characteristics of ACTH and cortisol secretion in control and naloxone-treated foetuses.The pattern of ACTH and cortisol secretion in saline-infused control foetuses was highly pulsatile but varied considerably between individual foetuses. ACTH pulses occurred on average every 40 min but were not always coincident with pulses of cortisol.There were no significant changes in average ACTH concentrations, pulse frequency or amplitude between foetuses sampled at 3 to 4 and 1 to 2 days before parturition, In contrast, average cortisol concentrations and pulse amplitude were significantly (P<0.05) increased, whereas pulse frequency was reduced, in foetuses at 1 to 2 days before parturition. Naloxone caused a significant (P < 0.05) inhibition of ACTH concentrations when compared with pretreatment values and with saline-treated controls, an effect which persisted for at least 2 h after the end of naloxone infusion. However, there were no significant differences during naloxone treatment in the frequency or amplitude of ACTH or cortisol pulses nor in the mean cortisol concentration. We conclude that ACTH and cortisol are secreted in a pulsatile fashion in the late gestation foetal sheep and that these pulses are not always coincident with each other. Blockade of endogenous opioid activity during the preparturient increase in pituitaryadrenal activity in foetal sheep, results in a reduction in plasma concentrations of ACTH. These results therefore provide evidence for the tonic regulation of foetal pituitary-adrenal activity by endogenous opioids during the final days prior to birth in the sheep.In sheep, a dramatic preparturient increase in the activity of the roetal hypothalamo-pituitary-adrenal axis is pivotal to the onset of birth. However, the neuroendocrine mechanisms which control foetal pituitary-adrenal function in the sheep, are poorly understood (1). Indeed, there is scant information as to the nature of adrenocorticotrophin (ACTH) and cortisol secretion during this important stage of foetal development. In adult animals, ACTH m d cortisol secretion is pulsatile (2) and a complex interaction between a number of neurotransmitter and neuropeptide systems, regulate the activity of this axis (3). However, until...

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“…Regulation of the hypothalamic-pituitary-adrenal axis is primarily dependent upon the secretion of corticotropin-releasing factor (CRF-41) from nerve endings within the external zone of the median eminence into the hypophysial-portal circulation (1)(2)(3). While other intrinsically weaker secretagogues may participate in regulation of adrenocorticotropin (ACTH) secretion (I, [3][4][5], numerous lines of evidence suggest that the presence of CRF-41 is obligatory for stimulated ACTH secretion (1,3,6,7).…”

mentioning

confidence: 99%

“…While other intrinsically weaker secretagogues may participate in regulation of adrenocorticotropin (ACTH) secretion (I, [3][4][5], numerous lines of evidence suggest that the presence of CRF-41 is obligatory for stimulated ACTH secretion (1,3,6,7). The ability to measure immunoreactive (ir) CRF-41 levels in the relatively unperturbed subject would be of general and clinical utility.…”

mentioning

confidence: 99%

Lack of Correlation Between Immunoreactive Corticotropin‐Releasing Factor Concentration Profiles in Hypophysial‐Portal and Peripheral Plasma

Plotsky¹,

Otto²,

Toyama³

et al. 1990

J Neuroendocrinology

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Corticotropin-releasing factor (CRF-41) is the primary mediator of adrenocorticotropin secretion from the adenohypophysis. This 41-amino-acid peptide is synthesized in perikarya of the paraventricular nuclei, transported to nerve terminals in the external zone of the median eminence and released into the hypophysial-portal circulation. It is also synthesized in multiple extrahypothalamic and peripheral sites. In addition, immunoreactive (ir) CRF-41 is present in the systemic circulation, raising the possibility that systemic measurements might provide a useful index of hypothalamic irCRF-41 secretion. This hypothesis was tested in several rat models. Neither bilateral destruction of hypothalamic irCRF-41 producing perikarya, nor infundibular stalk transection altered peripheral plasma irCRF-41 concentration. Furthermore, central administration of norepinephrine, an agent previously shown to evoke irCRF-41 secretion into the portal circulation, was without effect on peripheral irCRF-41 concentration. Finally, while increased irCRF-41 levels in both the hypophysial-portal and the peripheral circulation were associated with nitroprusside-induced hypotension, bilateral paraventricular nuclei lesions blocked irCRF-41 secretion into the hypophysial-portal circulation without blunting the rise observed in the peripheral circulation. The source of peripheral irCRF-41 remains undetermined; however, the adrenals may be excluded as bilateral adrenalectomy failed to alter circulating irCRF-41 levels. Therefore, our observations do not support the concept that peripheral irCRF-41 levels provide a useful index of hypothalamic secretion of this peptide into the hypophysial-portal circulation under the conditions tested.

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Hypothalamic Control of Adrenocorticotropin Secretion: Advances since the Discovery of 41-Residue Corticotropin-Releasing Factor

Cited by 923 publications

References 110 publications

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress

Effects of Naloxone on the Preparturient Increase in Adrenocorticotrophin and Cortisol in Foetal Sheep

Lack of Correlation Between Immunoreactive Corticotropin‐Releasing Factor Concentration Profiles in Hypophysial‐Portal and Peripheral Plasma

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