Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma cortisol, adrenocorticotrophic hormone (ACTH), beta-endorphin and corticotrophin releasing hormone or factor (CRF) all rise progressively as pregnancy advances, and fall postnatally. The placenta produces large amounts of CRF in the third trimester and this is released into the maternal circulation. Present evidence suggests that it stimulates the maternal pituitary to produce ACTH while desensitizing the maternal pituitary to further stimulation with CRF. Maternal control of ACTH production is retained, allowing a persistent response to stress and a diurnal rhythm, perhaps through the secretion of vasopressin. The placenta also produces pro-opiomelanocortin peptides; however, the nature of the fragments produced from the precursor differs from that formed in the anterior pituitary of the mother and the role of these fragments in the control of maternal adrenal function is unclear. These changes in the hypothalamo-pituitary-adrenal axis during pregnancy are associated with loss of the normal suppression of cortisol by dexamethasone and elevated basal levels of cortisol with preservation of a diurnal rhythm, features also found in some patients with endogenous depression. Several studies have suggested a relationship between alterations in maternal concentrations of cortisol and beta-endorphin and the development of postnatal mood disturbances.
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PMID:Neuroendocrinology of the hypothalamo-pituitary-adrenal axis in pregnancy and the puerperium. 203 26

This review examines the role of serotonin (5-HT) in depression. Dysfunction of serotonergic neurons has been implicated as one of the causes of endogenous depression. Since serotonergic neurons innervate the hypothalamus and these neurons send collaterals to several other brain areas, it is possible that hypothalamic sites which control hormone secretion receive the same serotonergic afferents that innervate other limbic areas in the brain. Several investigators have devised neuroendocrine challenge tests measuring the effect of 5-HT agonists on plasma cortisol and prolactin in depressed patients. These tests help to identify dysfunctional 5-HT neurons, and are a "window into the brain." The secretion of cortisol and prolactin is increased predominantly by 5-HT1 receptors. However, changes in 5-HT2 receptors have also been implicated in depression. Results from our laboratory and by others suggest that brain serotonergic neurons stimulate renin and vasopressin secretion by activation of 5-HT2 receptors. Therefore, the renin and vasopressin response to 5-HT agonists should be included in neuroendocrine tests of serotonergic function in affective disorders. Since antidepressants produce a decrease in the density of 5-HT2 receptors, renin and vasopressin could be used to evaluate the antidepressant potential of new drugs.
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PMID:Neuroendocrine aspects of the serotonergic hypothesis of depression. 269 29

Concentrations of the amines and amine metabolites dopamine (DA), noradrenaline (NA), adrenaline (A), serotonin (5-HT), homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG), 5-hydroxyindoleacetic acid (5-HIAA) and of the peptides, vasopressin (AVP), vasoactive intestinal polypeptide (VIP), thyrotropin releasing hormone (TRH) and cholecystokinin (CCK) were measured in lumbar cerebrospinal fluid (CSF) in patients with depression and compared with that of controls. Diagnostic classifications were performed according to ICD-9 and the Newcastle Rating Scales for Depression. The severity of depression was measured by Bech-Rafaelsen melancholia scale. Significantly decreased concentrations of CSF-A and AVP were found in as well endogenous as in non-endogenous depression, whereas reduced levels of CSF-VIP were found only in the non-endogenous group. CSF-5-HT and DA were significantly increased in endogenously depressed patients. In these studies patients with non-endogenous depression were not included. No relationship between severity of depression and concentrations of neurotransmitters was found. For most of the neurotransmitters no correlation between concentrations measured at the lumbar and at the ventricular level seems to exist. This finding indicates that measurements on CSF collected from the lumbar sack not necessarily are indicative for concentrations measured at more central levels. Although several transmitter systems most likely are disturbed in depression, results from studies on lumbar CSF should be interpreted with precaution, until further information about origin and distribution of neurotransmitters in CSF has been obtained.
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PMID:Do concentrations of neurotransmitters in lumbar CSF reflect cerebral dysfunction in depression? 290 16

Cerebrospinal fluid (CSF), thyrotropin releasing hormone (TRH), CSF-vasopressin (AVP), plasma-AVP, CSF-osmolality, plasma-osmolality, CSF-adrenaline (A) and -noradrenaline (NA) were measured in psychiatric patients and controls. Psychiatric patients were classified according to ICD-9 and grouped into endogenous depression, non-endogenous depression, mania and schizophrenia. The depressive groups were classified according to the Newcastle Rating Scale for Depression 1965. Severity of disease was quantified by BRMES, BRMS and BPRS. No difference in CSF-TRH levels was seen among the different diagnostic groups and controls. A positive correlation between CSF-TRH and CSF-A was demonstrated. CSF-AVP concentrations were significantly lowered in both endogenous and non-endogenous depression; no correlation with CSF-A or -NA was seen. Neither did any difference between plasma levels of AVP, plasma-osmolality or CSF-osmolality appear among the groups investigated.
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PMID:Cerebrospinal fluid vasopressin--changes in depression. 393 7

Psychiatric patients suffering from anxiety disorders or endogenous depression exhibit increased activity in their hypothalamo-pituitary-adrenocortical (HPA) axis. Recently, two Wistar rat lines, bred for high (HAB) and low (LAB) anxiety-related behaviour on the elevated plus-maze, were described as a unique psychopathological animal model (1). The present study focused on the HPA axis reactivity of HAB and LAB animals to an emotional stressor. Thus, adult male HAB and LAB animals, fitted with jugular vein catheters 5 days prior to the experiment, were exposed to an open arm of the elevated plus-maze for 5 min. Whereas basal levels of ACTH and corticosterone were similar in both lines, HAB rats showed higher plasma concentrations at 5 and 15 min following stressor exposure (both hormones and both time points: P<0.01 vs LAB). Furthermore, increased basal (P<0.05 vs LAB) and stimulated (P<0.01 vs LAB) prolactin concentrations in HAB rats were found. In contrast to ACTH, corticosterone and prolactin, plasma oxytocin and vasopressin levels did not differ between HAB and LAB animals; oxytocin, but not vasopressin, responding to open arm exposure with a significant increase in both lines (P<0.05). In conclusion, particularly due to the association between inborn anxiety and HPA axis hyper-reactivity, the HAB rat represents a promising animal model for further investigation of the relationship between emotional disturbance and neuroendocrine activity.
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PMID:Hyper-reactive hypothalamo-pituitary-adrenocortical axis in rats bred for high anxiety-related behaviour. 1033 20

The viral transneuronal labeling method was used to examine whether the suprachiasmatic nucleus (SCN) is linked by multisynaptic connections to the medial prefrontal cortex of the rat. In separate experiments, pseudorabies virus (PRV) was injected into one of the three different cytoarchitectonic regions that comprise the medial prefrontal cortex: infralimbic (Brodmann area 25), prelimbic (Brodmann area 32), and cingulate (Brodmann area 24) cortical areas. After 4-days survival, extensive SCN transneuronal labeling was found following infralimbic cortex (ILC) injections, but almost none occurred when the PRV injections were centered in the prelimbic or cingulate areas. In the ILC cases, transneuronal labeling was localized mainly in the dorsomedial SCN, although a moderate number of labeled neurons were found in the ventrolateral SCN. About 13% of the infected neurons were vasopressin immunoreactive and 4% were vasoactive intestinal polypeptide-positive. Another set of experiments was performed in which the paraventricular thalamic nucleus (PVT) was destroyed 2 weeks prior to making PRV injections into the ILC. Almost no SCN transneuronal labeling occurred in these animals, suggesting that the SCN projection to the ILC is dependent on a relay in the PVT. We propose that the SCN sends timing signals, via its relay in the PVT, to the ILC. This pathway may modulate higher-level brain functions, such as attention, mood, or working memory. Assuming that a homologous circuit exists in humans, we speculate that neurochemical changes affecting this pathway may account for some of the symptoms associated with clinical depression and attention-deficit/hyperactivity disorder.
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PMID:Suprachiasmatic nucleus projection to the medial prefrontal cortex: a viral transneuronal tracing study. 1237 60

Previous studies in the field of melancholic or endogenous depression have resulted in support for a subcategory of depression with above-normal plasma vasopressin (AVP) concentration (ANA). Since an analogous animal model with increased release of above-normal plasma vasopressin exhibits reduced Sympathetic-Nervous-System activity, the present study investigated the plasma norepinephrine concentration and the correlation between plasma norepinephrine and AVP in this ANA depression. As psychotic-melancholic patients may have increased plasma norepinephrine concentration, and noradrenergic activation may stimulate AVP release, potentially confounding effects of psychotic features were also investigated. The data set of the same depressed patient sample that was used before, but limited to those with complete hormonal data (n = 75), was re-analysed. ANA depression (n = 14) had negatively correlating AVP and norepinephrine concentrations. A very small subcategory of ANA depression with psychotic features (n = 3) had high plasma norepinephrine concentration, suggesting that this could be an independent subcategory. This was supported by the combination of relatively low above-normal plasma AVP concentrations with the highest severity scores for depression in this subcategory, which does not correspond with the positive correlation between AVP concentration and severity in non-psychotic ANA depression. The results further support the validity of ANA depression and the analogy with the High Anxiety Behaviour animal model of depression. Further investigations are needed to replicate these findings and to search for genetic and traumatic factors involved.
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PMID:Evidence of vasopressinergic-noradrenergic mechanisms in depression with above-normal plasma vasopressin concentration with and without psychotic features. 1994 36