Interaction of Stress, Corticotropin-Releasing Factor, Arginine Vasopressin and Behaviour

Beurel, Eléonore; Nemeroff, Charles B.

doi:10.1007/7854_2014_306

Cited by 52 publications

(23 citation statements)

References 115 publications

(118 reference statements)

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“…Indeed, the increased PVN Fos-ir in our study might be attributed to cell types that we did not measure like corticotropin-releasing hormone (CRH). CRH is the major neuropeptide that controls pituitary ACTH secretion in response to stress in adult animals (Beurel and Nemeroff 2014; Lightman 2008). Thus, elevated Fos-ir expression might relate to PVN CRH-neuron activation.…”

Section: Discussionmentioning

confidence: 99%

Rapid nonapeptide synthesis during a critical period of development in the prairie vole: plasticity of the paraventricular nucleus of the hypothalamus

2018

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Vasopressin (VP) and oxytocin (OT) are involved in modulating basic physiology and numerous social behaviors. Although the anatomical distributions of nonapeptide neurons throughout development have been described, the functional roles of VP and OT neurons during development are surprisingly understudied, and it is unknown whether they exhibit functional changes throughout early development. We utilized an acute social isolation paradigm to determine if VP and OT neural responses in eight nonapeptide cell groups differ at three different stages of early development in prairie voles. We tested pups at ages that are representative of the three rapid growth stages of the developing brain: postnatal day (PND)2 (closed eyes; poor locomotion), PND9 (eye opening; locomotion; peak brain growth spurt), and PND21 (weaning). Neural responses were examined in pups that (1) were under normal family conditions with their parents and siblings, (2) were isolated from their parents and siblings and then reunited, and (3) were isolated from their parents and siblings. We found that VP and OT neural activity (as assessed via Fos co-localization) did not differ in response to social condition across development. However, remarkably rapid VP and OT synthesis in response to social isolation was observed only in the paraventricular nucleus of the hypothalamus (PVN) and only in PND9 pups. These results suggest that PVN nonapeptide neurons exhibit distinct cellular properties during a critical period of development, allowing nonapeptide neurons to rapidly upregulate peptide production in response to stressors on a much shorter timescale than has been observed in adult animals.

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Section: Discussionmentioning

confidence: 99%

Rapid nonapeptide synthesis during a critical period of development in the prairie vole: plasticity of the paraventricular nucleus of the hypothalamus

2018

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“…The formation of heteromers of CRHRs with other GPCRs have been proposed to govern the integration of different signal transduction systems in complex biological responses, such as HPA activation, anxiogenic behavior and drug abuse. CRH effect at the pituitary level is amplified by arginine vasopressin (AVP), which is produced in the supraoptic nucleus and PVN, co-expressed and co-secreted from hypothalamic CRH neurons ( 52 , 53 ). Both CRH and AVP neurohormones trigger different signaling pathways in pituitary corticotrophs, but the cellular mechanism underlying the synergistic effect of CRH and AVP on ACTH release is not completely understood.…”

Section: Structural and Functional Features Of Crh And Urocortins Andmentioning

confidence: 99%

Endocrinology and the brain: corticotropin-releasing hormone signaling

Inda

Armando

Claro

et al. 2017

Endocrine Connections

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Corticotropin-releasing hormone (CRH) is a key player of basal and stress-activated responses in the hypothalamic–pituitary–adrenal axis (HPA) and in extrahypothalamic circuits, where it functions as a neuromodulator to orchestrate humoral and behavioral adaptive responses to stress. This review describes molecular components and cellular mechanisms involved in CRH signaling downstream of its G protein-coupled receptors (GPCRs) CRHR1 and CRHR2 and summarizes recent findings that challenge the classical view of GPCR signaling and impact on our understanding of CRHRs function. Special emphasis is placed on recent studies of CRH signaling that revealed new mechanistic aspects of cAMP generation and ERK1/2 activation in physiologically relevant contexts of the neurohormone action. In addition, we present an overview of the pathophysiological role of the CRH system, which highlights the need for a precise definition of CRHRs signaling at molecular level to identify novel targets for pharmacological intervention in neuroendocrine tissues and specific brain areas involved in CRH-related disorders.

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“…Indeed, a similar degree of suppression of the ACTH response to CRH has been reported for patients after surgical treatment for Cushing’s syndrome and for patients after withdrawal of ≥ 2 weeks of therapeutic glucocorticoid treatment [18, 26]. The suppressed ACTH responses to CRH observed in the subacute/prolonged phases of critical illness is compatible with low endogenous CRH and/or low vasopressin signaling [27], that both can be suppressed by high circulating levels of glucocorticoids [7]. Of note, baseline plasma ACTH concentrations were not completely suppressed and slightly increased over time.…”

Section: Discussionmentioning

confidence: 56%

ACTH and cortisol responses to CRH in acute, subacute, and prolonged critical illness: a randomized, double-blind, placebo-controlled, crossover cohort study

et al. 2018

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PurposeLow plasma ACTH in critically ill patients may be explained by shock/inflammation-induced hypothalamus-pituitary damage or by feedback inhibition exerted by elevated plasma free cortisol. One can expect augmented/prolonged ACTH-responses to CRH injection with hypothalamic damage, immediately suppressed responses with pituitary damage, and delayed decreased responses in prolonged critical illness with feedback inhibition.MethodsThis randomized, double-blind, placebo-controlled crossover cohort study, compared ACTH responses to 100 µg IV CRH and placebo in 3 cohorts of 40 matched patients in the acute (ICU-day 3–6), subacute (ICU-day 7–16) or prolonged phase (ICU-day 17–28) of critical illness, with 20 demographically matched healthy subjects. CRH or placebo was injected in random order on two consecutive days. Blood was sampled repeatedly over 135 min and AUC responses to placebo were subtracted from those to CRH.ResultsPatients had normal mean ± SEM plasma ACTH concentrations (25.5 ± 1.6 versus 24.8 ± 3.6 pg/ml in healthy subjects, P = 0.54) but elevated free cortisol concentrations (3.11 ± 0.27 versus 0.58 ± 0.05 µg/dl in healthy subjects, P < 0.0001). The order of the CRH/placebo injections did not affect the ACTH responses, hence results were pooled. Patients in the acute phase of illness had normal mean ± SEM ACTH responses (5149 ± 848 pg/mL min versus 4120 ± 688 pg/mL min in healthy subjects; P = 0.77), whereas those in the subacute (2333 ± 387 pg/mL min, P = 0.01) and prolonged phases (2441 ± 685 pg/mL min, P = 0.001) were low, irrespective of sepsis/septic shock or risk of death.ConclusionsSuppressed ACTH responses to CRH in the more prolonged phases, but not acute phase, of critical illness are compatible with feedback inhibition exerted by elevated free cortisol, rather than by cellular damage to hypothalamus and/or pituitary.Electronic supplementary materialThe online version of this article (10.1007/s00134-018-5427-y) contains supplementary material, which is available to authorized users.

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Interaction of Stress, Corticotropin-Releasing Factor, Arginine Vasopressin and Behaviour

Cited by 52 publications

References 115 publications

Rapid nonapeptide synthesis during a critical period of development in the prairie vole: plasticity of the paraventricular nucleus of the hypothalamus

Rapid nonapeptide synthesis during a critical period of development in the prairie vole: plasticity of the paraventricular nucleus of the hypothalamus

Endocrinology and the brain: corticotropin-releasing hormone signaling

ACTH and cortisol responses to CRH in acute, subacute, and prolonged critical illness: a randomized, double-blind, placebo-controlled, crossover cohort study

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