Plasmatic vasopressin neurophysin in depression: Basic levels and relations with HPA axis

Laruelle, Marc; Seghers, Arlette; Goffinet, S.; Bouchez, Stefaan; Legros, Jean-Jacques

doi:10.1016/0006-3223(90)90423-y

Cited by 13 publications

(3 citation statements)

References 44 publications

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“…For example, the levels of vasopressin and a-MSH are lower in depressed patients, particularly those with melancholia (Laruelle, Seghers, Goffinet, Bouchez, & Legros, 1990;Maes, DeJonckheere, Vandervorst, Schotte, Cosyns, Raus, & Suy, 1991), Paradoxically, acute infection occurring during severe depression may produce (in addition to exacerbated depressive symptoms) a rebound activation of the anti-inflammatory system, which could temporarily attenuate the depressive symptomatology. The effects of acute endotoxin injection on depressed patients was recently examined (Bauer, Hohagen, Gimmel, Bruns, Lis, Krieger, Ambach, Guthmann, Grunze, Fritsch-Montero, Weissbach, Ganter, Frommnerger, Riemann, & Berger, 1995); as found, proinflammatory cytokines levels and body temperature were elevated during the first 6hr following the injection, and the patients "exhibited pronounced apathy".…”

Section: Adaptive and Maladaptive Aspects Of Immunologically-induced mentioning

confidence: 96%

Cytokines, “Depression Due to A General Medical Condition,” and Antidepressant Drugs

Raz

Weidenfeld

Pollak

et al. 1999

Advances in Experimental Medicine and Biology

180

118

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Section: Adaptive and Maladaptive Aspects Of Immunologically-induced mentioning

confidence: 96%

Cytokines, “Depression Due to A General Medical Condition,” and Antidepressant Drugs

Raz

Weidenfeld

Pollak

et al. 1999

Advances in Experimental Medicine and Biology

180

118

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“…Indeed, the second notion is supported by the complete lack of a stimulatory action of AVP in perifusions of hypothalami from ADX/CB-replaced rats. Interestingly, a re cent clinical study concluded that impairments in AVP trans mission might occur in depressive disorders in which hypercortisolism is a common occurrence [48].…”

Section: Discussionmentioning

confidence: 99%

Adrenalectomy and Experimental Hypercorticalism Modulate the Basal, Corticotropin-Releasing-Hormone- and Arginine-Vasopressin-Stimulated Release of Hypothalamic Beta-Endorphin

1991

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Recent in vitro studies have shown that the release of hypothalamic β-endorphin (β-END), like that of adenohypo-physial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic β-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of β-END from the rat hypothalamus. Basal release of β-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10^–8 M) upon β-END release. ADX caused no significant change in the AVP (10^–6 M)-induced release of β-END. However, the AVP-stimulated release of β-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of β-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of β-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment. There was a tendency for hypothalamic levels of AVP to decrease and increase in ADX rats and CB-treated ADX rats, respectively. On the other hand, in the in vitro study, basal release of AVP was significantly increased and decreased in ADX and ADX/CB-supplemented rats, respectively. We conclude that hypothalamic β-END synthesis and basal release, as well as the efficacy of two of the endogenous secretagogues of β-END release, are determined by a fine balance in the levels of circulating glucocorticoids.

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“…This is diminished in depressed pa tients despite their normal basal concentrations of vaso pressin [27], Interestingly, however, basal plasma levels of vasopressin-neurophysin (hNp!) are significantly lower than normal in patients suffering from major depression [28]. Vasopressin levels in the CSF also seem to be reduced in depressed patients, though no relationship has been found between the intensity of the clinical depres sion and the decrease in vasopressin concentration [29], Vasopressin-neurophysin is also reduced in the CSF of patients with major depression [30],…”

Section: Major Depressionmentioning

confidence: 99%

Neurohypophyseal Peptides and Psychopathology

Legros¹

1992

Horm Res

Self Cite

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The study of neurohypophyseal peptides in various neuropsychiatric disorders is of interest because the hypothalamo-posterior pituitary axis is directly influenced by modifications of central neurotransmitter metabolism involved in behaviour control. Moreover, the main neurohypophyseal peptides, namely vasopressin and oxytocin, are themselves capable of modifying behaviour. In this paper the author discusses current understanding of the anatomy and physiology of the main central vasopressinergic and oxytocinergic pathways, followed by a description of the principal actions of exogenously administered vasopressin and oxytocin on human behaviour. Finally, modifications of endogenous neurohypophyseal function encountered in different pathological states are described.

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Plasmatic vasopressin neurophysin in depression: Basic levels and relations with HPA axis

Cited by 13 publications

References 44 publications

Cytokines, “Depression Due to A General Medical Condition,” and Antidepressant Drugs

Cytokines, “Depression Due to A General Medical Condition,” and Antidepressant Drugs

Adrenalectomy and Experimental Hypercorticalism Modulate the Basal, Corticotropin-Releasing-Hormone- and Arginine-Vasopressin-Stimulated Release of Hypothalamic Beta-Endorphin

Neurohypophyseal Peptides and Psychopathology

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