Release of Vasopressin within the Rat Paraventricular Nucleus in Response to Emotional Stress: A Novel Mechanism of Regulating Adrenocorticotropic Hormone Secretion?

Wotjak, Carsten T.; Kubota, Masaharu; Liebsch, Gudrun; Montkowski, Alexandra; Holsboer, Florian; Neumann, Inga D.; Landgraf, Rainer

doi:10.1523/jneurosci.16-23-07725.1996

Cited by 220 publications

(144 citation statements)

References 56 publications

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“…and 12 noon. Three days after surgery microdialysis (3.3 l/ min; Ringer solution, pH 7.4) was performed in the right PVN (HAB: n ϭ 6, LAB: n ϭ 8) as described previously (Wotjak et al 1996b;Keck et al 2000). After perfusion without sampling for 3 h, two consecutive 30-min dialysates were collected and immediately stored on dry ice.…”

Section: Dex/crh Test In Male and Female Hab Rats And Lab Ratsmentioning

confidence: 99%

“…As an approach to study a differential activation of magnocellular and parvocellular AVP neurons in HAB and LAB rats, we used the detection of AVP-like immunoreactivity in the internal and external zone of the median eminence, which was indistinguishable in the two rat breeding lines. Therefore, increased intra-PVN release, and thus increased local synthesis of AVP in magnocellular neurons of this nucleus, might simply represent local compensatory mechanisms of the organism to counterregulate an HPA system that is hyperactive per se (Wotjak et al 1996b). Accordingly, secretion of AVP into the blood circulation is similar in HAB and LAB rats under basal conditions (Landgraf et al 1999), arguing against a general hyperactivity of the magnocellular AVP system in HAB rats.…”

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confidence: 99%

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Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Keck

Wigger

Welt

et al. 2002

Neuropsychopharmacology

157

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To investigate the neuroendocrine alterations linked to inborn emotionality in two Wistar rat lines selectively bred for either high (HAB) or low (LAB) anxiety-related behavior, we administered the combined dexamethasone (DEX)/corticotropin-releasing hormone (CRH)testNeuroendocrine studies provide strong indications that hyperactivity of central corticotropin-releasing hormone (CRH) circuits, resulting in a characteristic dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) system, plays a causal role in the symptomatology of affective and anxiety disorders (review: Keck and Holsboer 2001). The effects of CRH are modulated by vasopressin (AVP), which, after prolonged stress and in senescence, is increasingly coexpressed and secreted from hypothalamic CRH neurons in both humans and rodents (Antoni 1993;Tilders et al. 1993;Hatzinger et al. 2000;Keck et al. 2000). Similarly, increased numbers of CRH neurons that coexpress AVP mRNA have been found in the hypothalamus of depressed patients (Raadsheer et al. 1993;Purba et al. 1996). The excessive release of CRH and AVP into hypophysial portal blood is thought to increase the secretion of corticotropin (ACTH) from pituitary corticotrope cells, and this in turn to increase the release of corticosteroids from the adrenal gland. In this context, a variety of changes in HPA system regulation have been demonstrated in psychiatric disorders such as major depression, among them defective negative feedback of the HPA system, basal hypercortisolemia, inappropriate HPA suppression by the synthetic corticosteroid dexamethasone (DEX) and a paradoxical stimulation of ACTH secretion by CRH after DEX pretreatment (review: Holsboer and Barden 1996;Holsboer 2000). In depression, the combined DEX/CRH test, in which DEX-pretreated subjects receive a single dose of CRH, has proven to be the most sensitive tool for the detection of altered HPA regulation. Depending on age and gender, up to 90% of patients with depression show this neuroendocrine phenomenon (Heuser et al. 1994). Moreover, studies using the DEX/CRH test not only agree that normalization of an initial aberrance is predictive of a favorable treatment response but also corroborate other evidence that a persistent HPA abnormality correlates with chronicity or relapse (Heuser et al. 1996;Zobel et al. 1999). Since activation of corticosteroid receptors suppresses the synthesis and release of CRH and AVP from the hypothalamic paraventricular nucleus (PVN) , these findings are consistent with the hypothesis of functionally impaired corticosteroid receptor signaling in both depressed patients (Modell et al. 1997) and healthy subjects at genetic risk for depression Modell et al. 1998).As the mechanisms underlying the abnormal HPA reactivity in patients with certain psychiatric disorders are not fully understood, animal models are needed to further investigate the hypothesized linkage between these disorders and changes in the regulation of the HPA system. After several generations of selective breeding, we could establish ...

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Section: Dex/crh Test In Male and Female Hab Rats And Lab Ratsmentioning

confidence: 99%

mentioning

confidence: 99%

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Keck

Wigger

Welt

et al. 2002

Neuropsychopharmacology

157

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“…It has been proposed that primary physical stressors such as hypovolemia, hemorrhage, hypoglycemia or exercise increase AVP secretion (9,10), whereas predominant psychological stressors such as restraint stress, ether-vapor stress or forced swimming have minor or no effect (6, 11 -13). However, recent studies indicate that this is not necessarily true, since repeated psychological stress was found to increase the concentration of AVP in the PVN (14) or the median eminence (15) or gene expression of AVP in the PVN (16). Together, these findings indicate that both types of stress activate the hypothalamo -neurohypophysial system, which may not necessarily be reflected in elevated peripheral hormone levels (17,18).…”

Section: Introductionmentioning

confidence: 97%

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Jørgensen

Knigge²,

Kjær³

et al. 2002

European Journal of Endocrinology

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Objective: To investigate the involvement of serotonin (5-hydroxytryptamine -5-HT) receptors in mediation of stress-induced arginine vasopressin (AVP) and oxytocin (OT) secretion in male rats. Design: Experiments on laboratory rats with control groups. Methods: Different stress paradigms were applied after pretreatment with intracerebroventricular infusion of saline or different 5-HT antagonists. Results: Restraint stress (5 min), hypotensive hemorrhage or dehydration for 24 h increased AVP secretion fivefold and OT secretion threefold. Swim stress for 3 min had no effect on AVP secretion, but increased OT secretion threefold. Ether vapor or hypoglycemia had no effect on AVP or OT secretion. The restraint stress-induced AVP response was inhibited by pretreatment with the 5-HT 2Aþ2C antagonists ketanserin (KET) and LY-53857 (LY) and the 5-HT 3þ4 antagonist ICS-205930 (ICS), whereas the 5-HT 1A antagonist WAY-100635 (WAY) had no effect. The OT response to restraint stress was inhibited by WAY, KET and LY but not by ICS. KET and LY inhibited OT response to dehydration, and LY inhibited OT response to hemorrhage. Neither of the antagonists affected AVP responses to dehydration or hemorrhage, nor the swim stress-induced OT response.

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“…Furthermore, there are indications of altered emotional behaviour in lactating rats (Hard & Hansen, 1984;Walker et al 1995). Besides the well-described stress responses of the HPA axis there is also activation of the hypothalamo-neurohypophysial system (HNS), releasing either oxytocin or vasopressin or both from the neurohypophysis into blood, in response to various stressors (Lang, Heil, Ganten, Hermann, Unger & Rascher, 1983;Kasting, 1988;Wotjak, Kubota, Ganster, Liebsch, Neumann & Landgraf, 1996). During lactation, the stimulated oxytocin secretion is reduced in response to physical stress (Carter & Lightman, 1987;Lightman, 1992;Neumann, Pittman & Landgraf, 1995b;Walker et al 1995) and hyperosmotic or pharmacological stimulation (Patel, Chowdrey & Lightman, 1991;Koehler, McLemore, Tang & Summy-Long, 1993;Neumann, Landgraf, Bauce & Pittman, 1995a).…”

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confidence: 99%

Attenuated neuroendocrine responses to emotional and physical stressors in pregnant rats involve adenohypophysial changes

Neumann

Johnstone

Hatzinger

et al. 1998

The Journal of Physiology

341

244

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1. The responsiveness of the rat hypothalamo-pituitary-adrenal (HPA) axis and hypothalamo-neurohypophysial system (HNS) to emotional (elevated plus-maze) and physical (forced swimming) stressors and to administration of synthetic corticotrophinreleasing hormone (CRH) was investigated during pregnancy and lactation. In addition to pregnancy-related adaptations at the adenohypophysial level, behavioural responses accompanying the neuroendocrine changes were studied. 2. Whereas basal (a.m.) plasma corticosterone, but not corticotrophin (adrenocorticotrophic hormone; ACTH), levels were increased on the last day (i.e. on day 22) of pregnancy, the stress-induced rise in both plasma hormone concentrations was increasingly attenuated with the progression of pregnancy beginning on day 15 and reaching a minimum on day 21 compared with virgin control rats. A similar attenuation of responses to both emotional and physical stressors was found in lactating rats. 3. Although the basal plasma oxytocin concentration was elevated in late pregnancy, the stressinduced rise in oxytocin secretion was slightly lower in day 21 pregnant rats. In contrast to vasopressin, oxytocin secretion was increased by forced swimming in virgin and early pregnant rats indicating a differential stress response of these neurohypophysial hormones. 4. The blunted HPA response to stressful stimuli is partly due to alterations at the level of corticotrophs in the adenohypophysis, as ACTH secretion in response to CRH in vivo (40 ng kg¢, i.v.) was reduced with the progression of pregnancy and during lactation. In vitro measurement of cAMP levels in pituitary segments demonstrated reduced basal levels of cAMP and a lower increase after CRH stimulation (10 nÒ, 10 min) in day 21 pregnant compared with virgin rats, further indicating reduced corticotroph responsiveness to CRH in pregnancy. 5. The reduced pituitary response to CRH in late pregnancy is likely to be a consequence of a reduction in CRH receptor binding as revealed by receptor autoradiography.[ÁÂÇI]CRH binding in the anterior pituitary was significantly reduced in day 11, 17 and 22 pregnant rats compared with virgin controls. 6. Anxiety-related behaviour of the animals as revealed by the time on and entries into the open arms of the elevated plus-maze was different between virgin and pregnant rats with decreased number of entries indicating increased anxiety with the progression of pregnancy (except on pregnancy day 18). The emotional behaviour, however, was not correlated with the neuroendocrine responses. 7. The results indicate that the reduced response of the HPA axis to stressors described previously during lactation is already manifested around day 15 of pregnancy in the rat and involves physiological adaptations at the adenohypophysial level. However, alterations in stressor perception at higher brain levels with the progression of pregnancy may also be involved.

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Release of Vasopressin within the Rat Paraventricular Nucleus in Response to Emotional Stress: A Novel Mechanism of Regulating Adrenocorticotropic Hormone Secretion?

Cited by 220 publications

References 56 publications

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Vasopressin Mediates the Response of the Combined Dexamethasone/CRH Test in Hyper-anxious Rats Implications for Pathogenesis of Affective Disorders

Serotonergic involvement in stress-induced vasopressin and oxytocin secretion

Attenuated neuroendocrine responses to emotional and physical stressors in pregnant rats involve adenohypophysial changes

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