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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some inbred strains of rats showed behavioural differences in the forced swimming test, which is considered a putative animal model of depression. In the present work, the behavioural and physiological responses to forced swimming were studied in male and female rats of five inbred strains of rats: Brown-Norway (BN), Fischer 344 (FIS), Lewis (LEW), Spontaneously Hypertensive (SHR) and Wistar-Kyoto (WKY). Physiological measures were aimed at characterizing emotional reactivity, a very important issue which has usually been approached by studying a single endocrine system, and its relationship to the forced swimming behaviour. The four indices of reactivity to stress used were serum glucose, ACTH, corticosterone and prolactin. No behavioural differences between sexes were observed in the forced swimming test. In addition, BN and WKY rats showed passive behaviour compared with the other three strains, the FIS strain being the most active. Whereas only minor differences were found in the resting levels of the variables studied with regard to either sex or strain, pituitary-adrenal (PA) and glucose responses to 15 min forced swimming differed among sexes and strains. Stress-induced hyperglycaemia was lowest in WKY and highest in SHR, being lower in females than in males. The lowest ACTH and corticosterone responses to forced swimming were observed in LEW and the highest in FIS. Female rats showed a clearly higher PA response to stress in all strains. Prolactin response to stress was very similar between sexes and strains. It might thus be concluded that: (i) there are important inter-strain differences in the forced swimming behaviour, with no differences between sexes; (ii) the various physiological indices of emotional reactivity follow a different trend and no warranted conclusion on differences in emotional reactivity should be based upon a single endocrine system or even only upon physiological measures; (iii) we cannot be sure, therefore, whether or not there are differences in emotionality between the strains studied in spite of well-established inter-strains differences in the forced swimming behaviour.
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PMID:Comparison of the behavioural and endocrine response to forced swimming stress in five inbred strains of rats. 883 94

Hypertension is often cited as a risk factor for erectile dysfunction. To clarify the relation between hypertension and erectile dysfunction, we evaluated 32 consecutive hypertensive and 78 normotensive impotent men with respect to multiple potential determinants and parameters of erectile function, including medical and sexual history, depression, hormonal profile, penile nocturnal tumescence, penile vascular supply, and pudendal nerve conduction. The hypertensive men were older, had higher body mass index, and used more medications than the normotensive men. The groups were not different with respect to the prevalence of smoking and peripheral vascular disease, but the hypertensive men had a marginally higher rate of ischemic heart disease (P = .06). The prevalence of depression, abnormal nocturnal penile tumescence, anomalous pudendal nerve conduction, and impairment in arterial supply as determined by penile brachial index were similar in the two groups. Testosterone and bioavailable testosterone levels were lower in the hypertensive men. After stratification by age and body mass index, hypertensive men younger than 50 years with body mass index less than 30 kg/m2 had significantly lower testosterone levels (12.0 +/- 1.7 versus 21.3 +/- 1.4 nmol/L, P < .02) but not bioavailable testosterone levels (3.9 +/- 0.7 versus 6.4 +/- 0.7 nmol/L, P < .17) than the corresponding normotensive group. Prolactin, follicle-stimulating hormone, and luteinizing hormone levels of the two groups were not significantly different. Contrary to common belief and with the exception of lower circulating testosterone levels, the overall analysis showed little difference between hypertensive and normotensive men with respect to a wide range of classic determinants of erectile function. Direct study of the local vascular erectile apparatus appears necessary for further elucidation of the mechanisms underlying erectile dysfunction in hypertensive men.
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PMID:Erectile dysfunction in hypertensive subjects. Assessment of potential determinants. 890 35

Previous studies indicate a profound suppression of tumour necrosis factor alpha (TNF-gamma), IL-1 beta and IL-6 release capacity by peritoneal macrophage (PM phi), splenic macrophage (SM phi) and Kupffer cells (KC) during late sepsis. Such a loss of functional capacity may reduce the animal's ability to ward off infection. Prolactin is known to enhance monocyte, T- and B-lymphocyte immune responses under normal conditions and has beneficial effects on cell-mediated immunity after haemorrhage. In the respect, the dopamine antagonist, metoclopramide, has been reported to increase circulating prolactin levels. Nonetheless, it remains unknown whether prolactin or metoclopramide have any salutary effect on macrophage (M phi) cytokine gene expression following sepsis. To study this, male C3H/HeN mice were subjected to sepsis and immediately thereafter were treated with prolactin (100 micrograms/25 g body weight, s.c.), metoclopramide (100 micrograms/100 g BW, s.c.) or given saline. PM phi, SM phi and KC (only SM phi and KC in metoclopramide-treated animals) were isolated at 24 h after sepsis. The monolayers were stimulated with or without LPS 10 micrograms/ml for 1 h in vitro. Total RNA was extracted and mRNA was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). A significant depression of constitutive and inducible mRNA levels of IL-1 beta, IL-6 and TNF-alpha in all three M phi populations were observed, when compared with shams (with exception of KC IL-6 mRNA in unstimulated cells). Prolactin as well as metoclopramide treatment after the onset of sepsis caused significant elevation of constitutive and inducible cytokine gene expression in all macrophages examined. Thus, prolactin and metoclopramide enhance the depressed M phi gene expression and may be useful in improving cell-mediated immunity during sepsis.
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PMID:Effects of prolactin and metoclopramide on macrophage cytokine gene expression in late sepsis. 919 78

A study of 40 young patients (age 14-22 years) with DSM-III-R schizophrenia (without substance abuse) was conducted following a mean of 3.4 years of neuroleptic treatment. After failing on conventional agents in clinical trials lasting a mean of 2 years, 20 patients were prospectively maintained on open-label clozapine (mean 324 mg daily), and another 20 patients continued on typical neuroleptics (mean 465 mg chlorpromazine-equivalents daily). Patients were then sampled for biochemical measures and assessed for psychopathology (Brief Psychiatric Rating Scale, Scales for the Assessment of Positive/ Negative Symptoms) on six occasions at consecutive 6-week intervals-during maintenance treatment on clozapine or conventional neuroleptics. There were 22-fold interindividual differences in clozapine levels and also high intraindividual differences over time. Maintenance dosage was linearly related to plasma levels of clozapine and its metabolites. Prolactin levels were elevated with typical neuroleptics but not clozapine. Blood levels of serotonin, methoxyhydroxyphenylglycol (MHPG), norepinephrine, and epinephrine (but not dopamine) were significantly higher in clozapine-treated patients than in conventionally treated patients. Higher serotonin levels were associated with significantly fewer negative symptoms, whereas higher MHPG levels were correlated with less depression. These findings suggest involvement of norepinephrine and serotonin in the pathophysiology of schizophrenia (with depression associated with lower MHPG levels and negative symptoms associated with lower serotonin levels) and in the therapeutic actions of clozapine. Speculatively, a treatment strategy of targeting specific neurotransmitter systems might be based on the presence of specific symptoms in adolescents and young adults with schizophrenia.
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PMID:Correlated changes in symptoms and neurotransmitter indices during maintenance treatment with clozapine or conventional neuroleptics in adolescents and young adults with schizophrenia. 923 4

We investigated the sleep electroencephalogram (EEG) and the nocturnal secretion of prolactin and cortisol in 25 normal subjects and 12 male inpatients with major depression before treatment and after remission and drug withdrawal. In the depressed patients, sleep-EEG disturbances persisted after recovery, whereas the cortisol concentration decreased. Prolactin variables in the patients did not differ between the two time points (i.e. before treatment and after remission). Compared with the normal subjects, the patients had significantly higher cortisol concentrations. The above findings were not altered when age was used as a covariate in statistical analysis. Our data suggest that neither depression nor aging exerts distinct effects on prolactin secretion.
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PMID:Nocturnal secretion of prolactin and cortisol and the sleep EEG in patients with major endogenous depression during an acute episode and after full remission. 933 99

d-Fenfluramine, a specific 5-HT releasing agent without the catecholamine effects of d,l-fenfluramine, was used as a serotonergic neuroendocrine challenge in subjects with unipolar major depression. Prolactin and cortisol responses to 30 mg d-fenfluramine were measured in patients at baseline. Patients were then randomly assigned to treatment for 6 weeks with a specific noradrenergic reuptake inhibitor, a tricyclic antidepressant, or placebo. Response to antidepressant treatment was assessed, and patients underwent further testing with d-fenfluramine. Prolactin responses were increased by treatment, but this was independent of whether or not patients' depression responded to treatment. Seven patients were treated with a specific noradrenergic reuptake inhibitor. These patients showed a significant rise in 5-HT-mediated cortisol responses after treatment, independent of whether their depression improved. We conclude that antidepressants which selectively modify noradrenergic function also have effects on 5-HT function as measured by neuroendocrine testing.
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PMID:Do noradrenergic reuptake inhibitors affect serotonergic function in depression? 945 84

Prolactin provides us with a window to the brain in our quest for understanding the psychobiology of depression, since the regulation of its release involves some of the monamine neurotransmitter systems that have been implicated in the pathophysiology of depression. Investigation examining basal prolactin plasma concentrations in depressed patients, including assessments of the rhythm of prolactin release, have not provided clear, consistent findings. Further exploration of the precise mechanisms involved in serotonin-stimulated prolactin release should shed light on the pathophysiology of abnormal prolactin responsivity in depression, and by extension, the psychobiologic basis of depression.
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PMID:Psychoneuroendocrinology of depression. Prolactin. 967 Feb 30

(+/-)3,4-Methylene-dioxymethamphetamine (MDMA, or 'Ecstasy') effects on serotonin system function and behaviour in humans are unclear. Fifteen MDMA users, who did not have other drug dependencies or alcohol abuse, and had not used other drugs for prolonged periods, and 15 control individuals were included in a study to assess the biological and psychological changes after chronic use of MDMA. Prolactin and cortisol responses to D-fenfluramine challenge, clinical psychobehavioural changes, personality characteristics, including mood, aggressiveness and temperamental aspects, were evaluated 3 weeks after MDMA discontinuation. MDMA users had significantly reduced prolactin and cortisol responses in comparison with control individuals (p < 0.001 and p < 0.005, respectively). Dysphoria and mood changes were exhibited in seven individuals, tiredness in five and sensation-seeking behaviour in twelve at the clinical evaluation. Significantly higher scores were found in MDMA individuals than in control individuals for Minnesota Multiphasic Personality Inventory subscale for Depression, for Buss Durkee Hostility Inventory direct and guilt subscales, for Hamilton Depression Rating Scale and for novelty-seeking Tridimensional Personality Questionnaire subscale. Prolactin responses to D-fenfluramine stimulation area under the curve among MDMA users were negatively correlated with direct aggressiveness scores for Buss Durkee Hostility Inventory; a negative correlation between prolactin responses and novelty-seeking scores was also evidenced among MDMA users. These data suggest an association between serotonin system impairment and MDMA use in humans; in interpretation of these results, the possibility that serotonin deficit in MDMA individuals was partially related to a premorbid condition, in relationship with novelty-seeking behaviour and mood disorders, can not be excluded.
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PMID:Serotonergic function after (+/-)3,4-methylene-dioxymethamphetamine ('Ecstasy') in humans. 998 61

Libido is a comprehensive and yet elusive word that indicates basic human mental states--and their biological counterparts--involved in the beginning of sexual behavior. It has three main roots: biological, motivational-affective and cognitive. All these dimensions may be variably affected in the post menopause, contributing to a progressive decrease of sexual drive that parallels the process of aging. Loss of estrogens and, specifically, of androgens deprives female libido of major biological fuel. The effect of this loss is pervading, affecting the central nervous system, the sensory organs that are the major windows to environmental sexual stimuli and the quality of sexual response, central, peripheral non-genital and genital. Prolactin increase may further inhibit libido. Arousal disorders, dyspareunia, orgasmic difficulties, dissatisfaction, both physical and emotional, may contribute to a secondary loss of libido. Depression, anxiety and chronic stress, may interfere with central and peripheral pathways of the sexual response, reducing the quality of sexual function mostly in its motivational root. Relational conflicts and/or marital delusions and partner-specific problems, erectile deficit first, may contribute to the fading of sexual drive in the post-menopausal years. Well tailored HRT, including androgens in selected cases, may reduce the biological causes of loss of libido. A comprehensive treatment requires a balanced evaluation between biological and psychodynamic factors.
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PMID:Libido: the biologic scenario. 1075 59

Plasma prolactin levels following oral administration of the serotonin (5-HT) releasing agent, fenfluramine hydrochloride, have been extensively used to evaluate central serotonergic function in affective and related disorders. Cortisol responses to fenfluramine have generally been a less informative measure. In healthy subjects, prolactin release by fenfluramine is dose-dependent, blocked by antagonists of serotonin receptors of the 5-HT-2a/2c type, negatively correlated with age and increased in young females. In major depression, a preponderance of studies have found blunted prolactin responses compared to matched normal controls. Although a significant minority of studies have not found blunting, increased prolactin release has not been observed. The blunted prolactin release is not due to a deficient secretory capacity of pituitary lactotrophs and is congruent with other evidence for reduced central serotonergic function in major depression. Blunting of the prolactin response may be associated with severity of depression and with elevated baseline cortisol levels. Treatment with antidepressant drugs and electroconvulsive therapy has been reported to increase the prolactin response but this has not been replicated in all studies. Blunted prolactin responses to fenfluramine have been fairly consistently associated with impulsive aggression in different personality disorders and with severity of suicide attempts in depressed patients. A number of studies employing the fenfluramine challenge test (FCT) have been conducted in obsessive compulsive disorder but their results have been variable. Prolactin responses to fenfluramine may be enhanced in panic disorder and chronic fatigue syndrome but the number of studies in these conditions is small as is the case for seasonal affective disorder. Since the therapeutic administration of fenfluramine as an appetite suppressant has been suspended because of reports of cardiac complications, further use of this compound as a challenge agent is not anticipated. Future studies are likely to employ agents acting on specific serotonin receptors and should apply methodological insights from the use of the FCT, which are considered in this review. Use of concomitant brain imaging to evaluate the central effects of challenge agents directly is likely to become more prevalent and may supplant neuroendocrine challenge paradigms such as the FCT which have been remarkably heuristic but are limited in scope and methodologically complex.
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PMID:Evaluation of central serotonergic function in affective and related disorders by the fenfluramine challenge test: a critical review. 1128 46


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