Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single-stage total-hepatectomy model in the rat is described. This model was successful in simulating the anhepatic phase for at least 4 h, with continuous intravenous glucose infusion. Advantages of the technique used for total hepatectomy in this study include ease of production, and resolution of problems encountered in previous models such as embolism and high postoperative mortality. This model was employed to observe fluctuation of pancreatic peptide hormones and glucose clearance during the anhepatic phase. Plasma insulin levels in portal blood did not vary for 120 min after removal of the liver. However, transient glucagon hypersecretion and depression in reactive secretion of somatostatin were observed during the anhepatic phase. These observations led to the following conclusions: (1) the liver seems to play an important role in regulating correlations between pancreatic peptide hormones by being part of a feedback system, and (2) hypersecretion of glucagon in the early anhepatic phase may be the initial signal for liver regeneration in the totally hepatectomized rat.
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PMID:Fluctuation of pancreatic peptide hormones in total-hepatectomy model in the rat. 790 88

In most cases, depression involves the interaction of biological and psychosocial factors. The impact of biological factors seems to be more prominent in major depressive syndrome, where typical symptoms and signs such as decrease in weight, changes in libido, dysmenorrhea, and sleeping disorders cannot be explained on psychodynamic grounds alone. Some of the symptoms and signs typical of patients suffering from depression reflect a primary disorder of biochemical and neurophysiological functions and are not commonly found in other forms of psychic disturbances. Studies related to monoamine (noradrenaline, serotonin or 5-HT, dopamine) metabolism have assumed a major role in biochemical research into depression; this research now also includes studies on other central neurotransmitters such as GABA and glutamic acid, and neuropeptides like somatostatin and corticotropin-releasing factor (CRF). Several theories have been suggested for the biochemical background of depression, and these hypotheses can now be tested using new and sophisticated research methods. Recent progress in understanding receptor structure and function and the regulation of neuroendocrine functions will substantially increase our knowledge of the biological deviations in depression and eventually lead to better drugs and treatment strategies. In the following, current perspectives on the biology of depressive disorders are introduced. It seems clear that susceptibility to depression is linked with deviations in presynaptic and postsynaptic neurotransmitter turnover and function. These, in turn, may lead to alterations in other regulatory mechanisms, such as the neuroendocrine and immune systems.
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PMID:Biological aspects of depression. 791 94

1. The sympathetic superior cervical ganglia (SCG) provide innervation to the pineal gland and median eminence through the internal carotid nerve and to the thyroid and parathyroid glands through the external carotid nerve. 2. Postsynaptic activation in median eminence nerve endings shortly after superior cervical ganglionectomy (SCGx) was accompanied by a depression of LH and FSH release and by a 3-5 day delay in rat estrous cyclicity. A decrease in TSH and GH release and an increase in ACTH and prolactin release were also found. These effects were accompanied by a) an increase in medial basal hypothalamic (MBH) LHRH, TRH and GHRH, b) a decrease in MBH somatostatin, AVP and CRH, and c) a normal adenohypophyseal response to hypophysiotropic hormones. Neurohypophyseal AVP release decreased during degeneration of sympathetic nerve terminals in the neurohypophyseal lobe after SCGx. The effects were generally mediated by alpha 1-adrenoceptors and were pineal gland. 3. In thyroid and parathyroid tissue the following events were observed during the wallerian degeneration phase after SCGx: a) alpha 1-adrenoceptor inhibition of thyroxine (T4) release, b) alpha 1-adrenoceptor inhibition, together with beta-adrenoceptor stimulation, of calcitonin release, and c) alpha 1-adrenoceptor inhibition of parathyroid hormone release. Thyroid sympathetic nerves also modulate slow phenomena such as compensatory thyroid growth after partial thyroidectomy. 4. In rats subjected to cholinergic decentralization of the thyroid gland, a decrease of plasma T4 and an increase of plasma TSH, as well as an impaired goitrogenic and thyroid compensatory response were detectable. The calcitonin and PTH response to changes in calcium levels increased after regional parasympathetic denervation. 5. The results indicate that cervical autonomic nerves constitute a parallel pathway through which the brain communicates with the endocrine system.
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PMID:Peripheral neuroendocrinology of the cervical autonomic nervous system. 808 Dec 83

To further explore the differential effects of peripherally and centrally derived hypercortisolism on neurohormonal systems implicated in the pathophysiology of mood and cognitive disturbances, we examined the cerebrospinal fluid (CSF) concentrations of immunoreactive somatostatin (IR-SRIF) in patients with Cushing's disease and major depression and the relationship of these levels to CSF immunoreactive corticotropin-releasing hormone (CRH) concentrations and urinary free cortisol excretion. In particular, since CSF SRIF levels consistently have been shown to be reduced in depression, we wished to assess whether decreased centrally directed SRIF was more likely a primary or a secondary factor in the hypercortisolism of major depression. CSF SRIF levels were significantly reduced in 11 patients with documented Cushing's disease and in 1 patient with ectopic adrenocorticotropic hormone secretion as compared with both 41 healthy volunteers (19.4 +/- 2.9 vs. 37.4 +/- 1.5 pmol/l; p < 0.01) and 28 patients with major depression (30.2 +/- 2.4 pmol/l; p < 0.05), whose CSF SRIF levels were also significantly reduced as compared with controls (p < 0.05). CSF SRIF levels in the Cushing's disease patients correlated positively with CSF CRH (r = 0.64; p < 0.025), suggesting that either the sustained hypercortisolism in these patients and/or its suppression of central CRH secretion contributed to the reduction in SRIF. A more modest but significant correlation between CSF SRIF and CSF CRH was observed in the healthy volunteers (r = 0.37; d.f. = 37; p < 0.02); in the depressed patients, no linear relationship, but rather an inverted U-shaped relationship was found which significantly fit by a quadratic function (r2 = 0.90; d.f. = 22; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebrospinal fluid immunoreactive somatostatin concentrations in patients with Cushing's disease and major depression: relationship to indices of corticotropin-releasing hormone and cortisol secretion. 809 79

Immunoreactive-somatostatin (ir-SS) concentrations of the gastric mucosa and mood state in patients with functional dyspepsia were examined. The subjects were 12 patients with upper abdominal discomfort, nausea and/or vomiting (motility disorder group) and 14 patients complaining of upper abdominal pain (ulcer-like disorder group) for more than a month without any organic upper-gastrointestinal tract disease proven by endoscopy. These patients were compared with either an age- and sex-matched group of asymptomatic outpatients without any organic disease (control group: n = 26) or to a group of patients with peptic ulcer (n = 19). Somatostatin concentrations of the stomach were measured by radio-immunoassay, and the mood state of each subject was assessed by Manifest Anxiety Scale (MAS) and Self-rating Depression Scale test. Immunoreactive-somatostatin concentrations of the gastric mucosa were significantly higher in the ulcer-like disorder group than in the peptic ulcer, motility disorder or control group, and gastric juice levels were higher in the ulcer-like disorder group. The psychometric tests showed that the motility disorder group was more depressive than the ulcer-like disorder group, but there were no differences between the motility disorder, ulcer-like disorder and peptic ulcer group in MAS scores or environmental factors. These results indicate that there may be two different subgroups in functional dyspepsia influenced by both ir-SS concentration of the stomach and/or mood state.
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PMID:Immunoreactive-somatostatin concentrations of the human stomach and mood state in patients with functional dyspepsia: a preliminary case-control study. 810 48

Secretion of growth hormone (GH) is excessive in acromegaly, but also in a number of other pathological states such as anorexia nervosa, insulin-dependent diabetes mellitus (IDDM), liver cirrhosis, depression, renal failure and GH-insensitivity syndrome. Abnormalities in the neuroendocrine control of GH secretion and/or a state of insensitivity to GH contribute to hypersecretion of GH in these states, with the possible exception of acromegaly, which appears to be a primary pituitary disease. GH hypersecretion may also occur in neonates or adolescents with tall stature, thus reflecting particular physiological or paraphysiological conditions. In the cohort of brain neurotransmitters, catecholamines and acetylcholine reportedly play a major role in the control of neurosecretory GH-releasing hormone (GHRH) and somatostatin (SS)-producing neurons, and hence GH secretion. Activation of alpha 2-adrenoceptors or of muscarinic cholinergic receptors in the hypothalamus stimulates GH release, probably through stimulation of GHRH and inhibition of SS release, respectively. Activation of dopamine receptors likewise stimulates GH release, while activation of beta-receptors inhibits GH release through stimulation of hypothalamic SS function. This review discusses the involvement of brain catecholamines and acetylcholine in GH hypersecretory states, including anorexia nervosa, acromegaly, IDDM, liver cirrhosis, depression, renal failure and GH insensitivity syndrome, with a view to providing a fuller understanding of their pathophysiology and, whenever possible, diagnostic and therapeutic implications.
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PMID:Involvement of brain catecholamines and acetylcholine in growth hormone hypersecretory states. Pathophysiological, diagnostic and therapeutic implications. 858 28

Aspartic acid (580 mg/kg, SC) causes a long-lasting depression of ventilation in adult male, but not female rats. The purpose of these experiments was to determine if the aspartic acid-induced depression of ventilation in awake male Sprague-Dawley rats is a consequence of the release of endogenous opioids or somatostatin. These neuromodulators have been shown to cause depression of ventilation. Pretreatment of male rats with the opioid antagonist naloxone (5 mg/kg) 10 min prior to aspartic acid attenuated the drop of ventilation from -138.6 +/- 26.9 ml/min to -63.4 +/- 16.6 ml/min (p < 0.01) by affecting both tidal volume and frequency of breathing. Naloxone administered prior to saline had no effect on ventilation. In another experiment, cysteamine (100 mg/kg), a somatostatin depleter, injected SC 2 h before aspartic acid administration also attenuated depression of ventilation by affecting frequency of breathing. Cysteamine alone, compared to saline, had no effect on ventilation over 24 h. These results suggest that aspartic acid acts by releasing endogenous opioids and somatostatin.
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PMID:Cysteamine and naloxone attenuate aspartic acid-induced depression of ventilation. 877 56

The effect of stressful stimulation and protein malnutrition on the gonadotrophic and somatotrophic axis of sheep is discussed with special references to the relationship between these stimuli and the GnRH and somatostatin neuronal systems in the hypothalamus. Generally, long-term stimulation and chronic underfeeding reduce gonadal functions in the sheep. There is evidence for the GnRH-dependent pathway for the mechanism of these phenomena in female sheep. GnRH neurons respond to long-term stress in diminishing of neuropeptide release from the nerve terminals due to the depression of its axonal transport. Chronic restriction of dietary proteins in lambs reduces the plasma LH concentrations but does not impair the development of GnRH neurons nor the synthesis and processing of GnRH. It is suggested that malnutrition delays the first ovulation probably due to the neural mechanism responsible for the preovulatory GnRH/LH output. Stress has rather unclear effect on growth hormone (GH) secretion in the sheep. Prolonged, but not short stressful stimulation provokes the rapid release of somatostatin, which is sustained during long-term stimulation. These results suggest that effect of stress on somatotrophic axis depends on the period of stressful stimulation. Chronic malnutrition enhances secretion of GH by an increase in amplitude of GH pulses and reduces the secretory activity of somatostatin neurons. It is postulated that nutrients can influence GH secretion in the sheep by mechanism dependent on the hypothalamic somatostatin.
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PMID:Stress and nutritional influences on GnRH and somatostatin neuronal systems in the ewe. 891 8

Many neuromodulators inhibit N-type Ca2+ currents via G protein-coupled pathways in acutely isolated superior cervical ganglion (SCG) neurons. Less is known about which neuromodulators affect release of norepinephrine (NE) at varicosities and terminals of these neurons. To address this question, we used carbon fiber amperometry to measure catecholamine secretion evoked by electrical stimulation at presumed sites of high terminal density in cultures of SCG neurons. The pharmacological properties of action potential-evoked NE release paralleled those of N-type Ca2+ channels: Release was completely blocked by Cd2+ or omega-conotoxin GVIA, reduced 50% by 10 microM NE or 62% by 2 microM UK-14,304, an alpha2-adrenergic agonist, and reduced 63% by 10 microM oxotremorine M (Oxo-M), a muscarinic agonist. Consistent with action at M2 or M4 receptor subtypes, Oxo-M could be antagonized by 10 microM muscarinic antagonists methoctramine and tropicamide but not by pirenzepine. After overnight incubation with pertussis toxin, inhibition by UK-14,304 and Oxo-M was much reduced. Other neuromodulators known to inhibit Ca2+ channels in these cells, including adenosine, prostaglandin E2, somatostatin, and secretin, also depressed secretion by 34-44%. In cultures treated with omega-conotoxin GVIA, secretion dependent on L-type Ca2+ channels was evoked with long exposure to high K+ Ringer's solution. This secretion was not sensitive to UK-14,304 or Oxo-M. Evidently, many neuromodulators act on the secretory terminals of SCG neurons, and the depression of NE release at terminals closely parallels the membrane-delimited inhibition of N-type Ca2+ currents in the soma.
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PMID:Modulation by neurotransmitters of catecholamine secretion from sympathetic ganglion neurons detected by amperometry. 903 83

Depression frequently coexists with dementia, although in many cases the depression is not recognized clinically. Depression represents a major additional burden in dementia, not only for the patients but also for families, caregivers, and, economically, society as a whole. However, depression in patients with dementia does respond to treatment, and appropriate therapy can significantly improve the well-being of these patients. Depression in patients with dementia is currently treated with a variety of standard antidepressive agents (tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors), but none is free from significant side effects. Moreover, the use of these drugs is often complicated by a number of age-related factors or effects on the cholinergic neurotransmitter system. Consequently, an antidementia treatment with concomitant antidepressive properties and an acceptable benefit/risk ratio would represent an attractive therapeutic option. The pathogenesis of depression in patients with dementia is not well understood, but may be related to increased intracellular calcium ions in the CNS, the so-called "calcium hypothesis." This hypothesis may explain why some calcium antagonists exert psychotropic effects, including putative antidepressant activity. Animal models and clinical data provide support for the use of calcium channel antagonists for the treatment of depression, with the potential for good tolerability. The latter aspect is especially important for elderly patients with dementia. Although antidepressive effects have been seen with a number of calcium channel antagonists, the dihydropyridine derivative nimodipine shows particular potential for clinical use, perhaps because nimodipine is one of the most lipophilic of these drugs and therefore achieves high concentrations in the CNS, and because of the unique biochemical properties of the dihydropyridine compounds compared with other L type calcium channel blockers. Nimodipine also increases somatostatin levels in CSF, one of the cardinal biochemical deficits in Alzheimer's disease. Data obtained incidentally from the use of nimodipine in the treatment of elderly demented patients clearly demonstrate significant antidepressant activity by the drug in this patient group. Formal clinical evaluation is therefore recommended to establish more clearly the therapeutic benefits offered by nimodipine in patients who suffer from both dementia and depression.
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PMID:The management of coexisting depression in patients with dementia: potential of calcium channel antagonists. 903 70


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