Corticotropin‐Releasing Hormone Neurons in the Paraventricular Nucleus Project to the External Zone of the Median Eminence: A Study Combining Retrograde Labeling with Immunocytochemistry

Lennard, David E.; Eckert, William A.; Merchenthaler, Istvån

doi:10.1111/j.1365-2826.1993.tb00378.x

Cited by 37 publications

(26 citation statements)

References 27 publications

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“…In a PVH-lesioned rat, Ն90% of the hypophysiotropic CRH cells are eliminated, with some CRH-expressing neurons remaining in the medial preoptic area and the dorsal lateral hypothalamus near the fornix, just behind the PVH (22,34), and with CRH appearing in the supraoptic neurons (35). The extraparaventricular CRH mRNA changes were also illustrated in the present study.…”

Section: Discussionsupporting

confidence: 53%

Role of hypothalamic inputs in maintaining pituitary-adrenal responsiveness in repeated restraint

Zelena¹,

Mergl²,

Földes³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

104

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. Role of hypothalamic inputs in maintaining pituitary-adrenal responsiveness in repeated restraint. Am J Physiol Endocrinol Metab 285: E1110-E1117, 2003; 10.1152/ ajpendo.00219.2003.-The role of hypothalamic structures in the regulation of chronic stress responses was studied by lesioning the mediobasal hypothalamus or the paraventricular nucleus of hypothalamus (PVH). Rats were acutely (60 min) and/or repeatedly (for 7 days) restrained. In controls, a single restraint elevated the plasma adrenocorticotropin (ACTH), corticosterone, and prolactin levels. Repeated restraint produced all signs of chronic stress, including decreased body and thymus weights, increased adrenal weight, basal corticosterone levels, and proopiomelanocortin (POMC) mRNA expression in the anterior pituitary. Some adaptation to repeated restraint of the ACTH response, but not of other hormonal responses, was seen. Lesioning of the mediobasal hypothalamus abolished the hormonal response and POMC mRNA activation to acute and/or repeated restraint, suggesting that the hypothalamo-pituitaryadrenal axis activation during repeated restraint is centrally driven. PVH lesion inhibited the ACTH and corticosterone rise to the first restraint by ϳ50%. In repeatedly restrained rats with PVH lesion, the ACTH response to the last restraint was reduced almost to basal control levels, and the elevation of POMC mRNA level was prevented. PVH seems to be important for the repeated restraint-induced ACTH and POMC mRNA stimulation, but it appears to partially mediate other restraintinduced hormonal changes. adrenocorticotropin; corticosterone; mediobasal hypothalamus; paraventricular nucleus; proopiomelanocortin; rat IN ACUTE STRESS, the hypothalamic paraventricular nucleus of hypothalamus (PVH) is known to be a key site in the activation of the hypothalamo-pituitary-adrenal (HPA) axis by providing the hypophysiotropic neuropeptides corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) to stimulate ACTH secretion from the anterior pituitary (see Ref. 2). Various stress paradigms act through different pathways, because in some cases the elimination of PVH abolished acute stress-induced ACTH elevation [hemorrhage (10), early response after bacterial lipopolysaccharide (13), elevated platform stress (28)], but with some other stressors, considerable ACTH and/or corticosterone elevation occurs even after lesioning the PVH [hypovolemia (7), ether (8, 27, 29), immobilization, electrical stimulation of the skin (14), footshock, IL-1␤ (40)].Chronic stress can be elicited by repeated exposure to short-acting stressors or by action of a sustained or persistent stimulus, e.g., a disease. Chronic stress is characterized by the classical symptoms of decreased body and thymus weight and a parallel increase in adrenal size and width of the adrenal cortex, consistent with chronic activation of the HPA axis (6, 12). The sustained activation of the CRH/AVP cells in the PVH is suggested to have a central role during chronic stress-induced HPA axis activation, and t...

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Section: Discussionsupporting

confidence: 53%

Role of hypothalamic inputs in maintaining pituitary-adrenal responsiveness in repeated restraint

Zelena¹,

Mergl²,

Földes³

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

104

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“…Whereas it is generally accepted that pituitary ACTH secretion is stimulated by CRF secreted by neurons emanating from the parvocellular nucleus of the hypothalamus (Lennard et al, 1993), the absence of a correlation between the diurnal cycles of CSF CRF and plasma cortisol concentrations (Garrick et al, 1987;Kalin et al, 1987;Geracioti et al, 1997;Kling et al, 1994) is believed to indicate that most CSF CRF does not originate from the hypothalamus. Given the lengthy transit flow time of CSF through the central nervous system (CNS), the 10-min half-life of CRF within CSF suggests that a preponderance of the CRF present in lumbar CSF is secreted by the spinal cord (Geracioti et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Corticotropin-Releasing Factor (CRF) and Vasopressin Concentrations Predict Pituitary Response in the CRF Stimulation Test: A Multiple Regression Analysis

Newport

Heim

Owens

et al. 2002

Neuropsychopharmacol

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There is considerable evidence that stress-related psychiatric disorders, including depression and post-traumatic stress disorder (PTSD), are associated with hypersecretion of corticotropin-releasing factor (CRF) within the central nervous system (CNS). One line of evidence that is consistent with central CRF hypersecretion in these disorders is the blunted adrenocorticotropin hormone (ACTH) response to intravenous CRF administration, likely a consequence, at least in part, of downregulation of anterior pituitary CRF receptors. The present study tests the hypothesis that elevated cerebrospinal fluid (CSF) concentrations of CRF and a secondary ACTH secretagogue, arginine vasopressin (AVP), are associated with diminished adenohypophyseal responses in a standard CRF stimulation test. CSF concentrations of CRF and AVP, and plasma ACTH responses to the administration of 1 mg/kg ovine CRF (oCRF) were measured in healthy adult women with and without current major depression and/or a history of significant childhood abuse. The primary outcome measure was ACTH area under the curve (AUC) in the CRF stimulation test. Multiple linear regression was performed to identify the impact of CSF CRF and AVP concentrations upon the pituitary response to CRF stimulation. The regression model explained 56.5% of the variation in the ACTH response to CRF stimulation. The relationship of CSF concentrations of CRF to ACTH responses to CRF were best described by a third-order function that was inversely correlated over most of the range of studied values. The association of ACTH response with CSF concentration of AVP and the dose of oCRF followed second-order kinetics. These findings support the hypothesis that central CRF hypersecretion is associated with a blunted ACTH response to exogenously administered CRF, explaining almost 60% of the variation in the ACTH response to CRF.

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“…The axons of these cells run laterally and caudally and terminate in the outer zone of the median eminence to release CRH into the portal vasculature of the anterior pituitary to initiate the neuroendocrine stress response (Gibbs & Vale 1982, Lennard et al 1993.…”

Section: Introductionmentioning

confidence: 99%

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Kovács

2013

Journal of Chemical Neuroanatomy

105

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Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity towards the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.Key words: Corticotropin-releasing hormone, paraventricular nucleus, central amygdala, bed nucleus of stria terminalis, corticosterone, cAMP-response element.

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Corticotropin‐Releasing Hormone Neurons in the Paraventricular Nucleus Project to the External Zone of the Median Eminence: A Study Combining Retrograde Labeling with Immunocytochemistry

Cited by 37 publications

References 27 publications

Role of hypothalamic inputs in maintaining pituitary-adrenal responsiveness in repeated restraint

Role of hypothalamic inputs in maintaining pituitary-adrenal responsiveness in repeated restraint

Cerebrospinal Fluid Corticotropin-Releasing Factor (CRF) and Vasopressin Concentrations Predict Pituitary Response in the CRF Stimulation Test: A Multiple Regression Analysis

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

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