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)

This study was conducted to characterize the mechanisms of hyperglycaemia in exercising sheep. Sheep were run on a treadmill for 45 min (5.5 km h-1, 8% incline) during adrenergic blockade (propranolol or phentolamine mesylate infusions) and during suppression of the rise in glucagon by infusion of somatostatin (SRIF). Propranolol did not alter the glucagon, insulin or glucose responses, except it tended to increase the metabolic clearance of glucose, presumably as a result of blocking the beta-adrenergic inhibition of glucose uptake. Phentolamine mesylate administration was associated with a suppression of the rise in glucagon concentrations, a reversal of alpha-adrenergic inhibition of insulin release and a reduction in glucose appearance during exercise. SRIF prevented the rise in glucagon and reduced insulin concentrations to below resting values. Propranolol and phentolamine mesylate did not alter the glucagon, insulin or glucose response to SRIF. However, SRIF prevented the insulin rise that occurred during phentolamine administration. The increment in glucose appearance produced in response to exercise was the same for SRIF, plus phentolamine mesylate and phentolamine mesylate in the first 25 min of exercise, but was significantly less than in the controls. During the last 20 min of exercise, glucose appearance was not significantly different from the control for any of the groups. The depression by SRIF and alpha-adrenergic blockade of the increment in glucose appearance due to exercise was associated with an impairment of the glucagon response. It appears, therefore, that glucagon may stimulate glucose production early in exercise in sheep directly, as well as by having a permissive effect.
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PMID:Effects of somatostatin and adrenergic blockade on glucagon, insulin and glucose in exercising sheep. 612 38

Immunoreactive somatostatin, bombesin, and cholecystokinin were measured in cerebrospinal fluid of normal subjects and patients with anorexia nervosa, depression, mania, and schizophrenia. Somatostatin-like immunoreactivity was decreased in anorexic and depressed patients. Bombesin-like immunoreactivity tended to be decreased in schizophrenics. Cholecystokinin-like immunoreactivity did not differ between groups. These data suggest a possible function for neuropeptides in regulation of human behavior.
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PMID:Altered neuropeptide concentrations in cerebrospinal fluid of psychiatric patients. 612 76

Motilin, [Met]enkephalin, [Leu]enkephalin, somatostatin, taurine, gamma-aminobutyric acid (GABA), and glycine were tested for their effects on Deiters neurons of the lateral vestibular nucleus in rabbits. Iontophoresis was carried out with multibarrelled micropipettes. All four peptides and three amino acids produced depression of neuron firing. No facilitatory responses were observed. The depressant action of each peptide when iontophoresed alone was dose-dependent and was rapid in onset and recovery. Their characteristic actions suggest the possibility of their independent roles as strong inhibitors, although the experimental paradigm does not allow conclusions about the individual potency of each peptide. When GABA was administered together with motilin, [Met]enkephalin, or somatostatin, the effects of the peptide and GABA were additive, producing depression greater than that with application of either substance alone. When GABA was applied in conjunction with [Leu]enkephalin, more complex interactions were observed. At low iontophoretic currents, [Leu]enkephalin antagonized the action of GABA, producing a depression less than that of GABA alone and of considerably slower onset, suggesting an additional modulatory effect. These observations support the conclusion that all substances tested are chemical mediators in the lateral vestibular nucleus and [Leu]enkephalin may be a neuromodulator as well. Because recent immunocytochemical studies indicate that Purkinje cells in the cerebellar cortex are chemically heterogeneous and exhibit immunoreactivity for motilin, taurine, the enkephalins, and somatostatin, as well as for the GABA-synthesizing enzyme glutamic acid decarboxylase, it is suggested that the Purkinje cell projections to vestibular and cerebellar nuclei are multimodal in their chemical coding. The uniformly depressant action of the peptides and amino acids reported here is consistent with earlier observations that Purkinje cells exert an inhibitory influence on the vestibular and central cerebellar nuclei.
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PMID:Inhibitory effects of motilin, somatostatin, [Leu]enkephalin, [Met]enkephalin, and taurine on neurons of the lateral vestibular nucleus: interactions with gamma-aminobutyric acid. 612 70

Somatostatin treatment was administered to 20 psoriatic patients according to the following protocol: Continuous infusion (250 micrograms/h) for at least 2 days followed either by short infusions (1 h) at 8 A.M. and 8 P.M. (12 cases) or by repeating the initial 2-day infusion (eight patients). Before treatment (day 0) and on day 6, biopsy specimens were taken for routine examination (12 patients) and for ultrastructure (seven patients). In vitro immunological studies were carried out on peripheral blood lymphocytes (six patients) on day 0 and day 8. In two patients, somatostatin was stopped because of serious side effects. Thus, clinical results were evaluated in 18 patients, on day 30. In ten of them no improvement whatsoever occurred, two had a partial clearing and an almost complete remission was achieved in six others. Ultrastructural studies showed, on day 6, enlargement of the intercellular spaces with deposits of granular material of glucidic composition, associated with features of cellular damage. Percentages of T and B cells were unmodified but a significant depression of mitogenic stimulation by PHA and ConA was clearly observed on day 8. Even if somatostatin treatment may have a beneficial effect in some patients it seems much less valid than other well-known therapies for psoriasis.
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PMID:Somatostatin treatment of psoriasis. 613 49

Somatostatin is a hypothalamic tetradecapeptide with many actions. We investigated a potential role for somatostatinergic neuron dysfunction in affective disorder by measuring somatostatin in the CSF of 47 patients with affective illness and of 39 normal volunteers. Medication-free depressed patients showed significantly lower levels of CSF somatostatin than normal volunteers (P less than .001) or patients during the improved state (P less than .01). A significant inverse correlation was observed between somatostatin and the duration of sleep on the night of the lumbar puncture. We also observed significant correlations between somatostatin and 5-hydroxyindoleacetic acid and norepinephrine in the CSF. Also noted were the significance of depression-related decreases in CSF somatostatin in relation to information about central somatostatin secretion, reported abnormalities of somatostatin activity, and potential interactions between alterations in somatostatin activity and the pathophysiology of depression.
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PMID:CSF somatostatin in affective illness. 613 92

The hypothesis that depression of insulin and glucagon levels during rapid, acute hemorrhage is controlled by somatostatin was supported by hormonal changes measured in the cat. By 5 min of hemorrhage to 50 mmHg (1 mmHg = 133.322 Pa) arterial blood pressure, insulin and glucagon were severely depressed and somatostatin levels rose to 232% of basal levels. Insulin and glucagon suppression was maintained for the 30-min period of hemorrhage. Following return of the blood, somatostatin levels remained high and insulin and glucagon suppression was maintained. The data support, but do not prove, the hypothesis.
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PMID:A possible role for somatostatin in depression of insulin and glucagon levels during hemorrhage. 613 75

The effect of somatostatin on lateral hypothalamic self-stimulation was investigated in atropine- and methysergide-pretreated rats. Somatostatin markedly decreased the self-stimulation rate of the animals. Atropine in a dose which had no action on self-stimulation partly antagonized the effect of somatostatin. Methysergide potentiated the somatostatin-induced depression of self-stimulation behavior. These results suggest that the central cholinergic and serotoninergic systems may play a role in the somatostatin-induced inhibition of self-stimulation.
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PMID:The effect of somatostatin on self-stimulation behavior in atropine- and methysergide-pretreated rats. 613 93

The prevalence of severe dementia in the United States is about 1.3 million cases, of which at least 50 to 60% are of the Alzheimer type. Severe dementia of the Alzheimer type is found rarely in a clearly dominant pattern, although often one or more relatives are affected. Down's syndrome in adults is often associated with Alzheimer changes. The diagnosis is a clinicopathological one; there is a considerable error rate in the clinical diagnosis early in the course of the disease, especially in regard to dementia in depression. The differential diagnosis involves a great many disorders, including multi-infarct dementia, tumors, subdural hematomas, and others. Physiological aspects of Alzheimer's disease include a diffusely slow electroencephalogram, reduced cerebral blood flow, and particular patterns noted on positron emission tomographic scanning. The latter technique has also demonstrated that oxygen extraction is normal in Alzheimer's disease, thus excluding ischemia from possible pathogenetic factors. Morphological changes, that is, the presence of plaques and tangles, are widely distributed in neocortex, paleocortex, and many deep gray areas down through the pontine tegmentum, but largely exclude the basal ganglia, thalamus, and substantia nigra. Numerous plaques without neocortical tangles are found in many demented persons older than 75 years. A severe loss of large neocortical neurons is characteristic of the disease. The chemical nature of the paired helical filaments that make up the neurofibrillary tangle has not yet been ascertained. Neurons are markedly deficient in the basal forebrain nuclei, and this deficiency may account for the severe diminution of choline acetyltransferase and acetylcholine in the neocortex and paleocortex. Muscarinic cholinergic receptors are present in normal amounts. Norepinephrine is reduced in some cases, and somatostatin in most. Substance P is low in severe cases. The etiology of the disorder is unknown and the role of aluminum is disputed. Management of patients with Alzheimer's disease is difficult, and neuroleptics are to be used with great caution because of their side effects. Substrate therapy has not been effective; physostigmine improves memory but is not suitable for general use. Trophic factors, gangliosides, and aluminum chelation are being investigated for use in pharmacological intervention.
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PMID:Senile dementia of the Alzheimer type. 613 75

The effects of hypoxia and hypercapnea in the production of somatostatin (SRIF)-induced apnea were studied during rebreathing experiments. Hypoxia and hypercapnea resulted in a shortening of the latency of SRIF-induced apnea. In order to exclude the effect of stimulation of central chemoreceptors by mock-CSF solution, control experiments using mock-CSF in combination with hypoxia and hypercapnea were done. No apnea could be produced by the mock-CSF in combination with hypoxia and hypercapnea. The shortening of apneic latency from 480 +/- 8 s (S.E.M.) to 148 +/- 30 s with the addition of a chemostimulus (hypoxia and hypercapnea) in SRIF-induced respiratory depression demonstrates that chemostimulation interacts with the centrally originating apnea to enhance its apneic response.
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PMID:Somatostatin-induced apnea: interaction with hypoxia and hypercapnea in the rat. 614 5

Somatostatin-like immunoreactivity was measured in the cerebrospinal fluid (CSF) of 85 inpatients with current or recent episodes of major depressive disorders, diagnosed according to Research Diagnostic Criteria (RDC) as assessed with the Schedule for Affective Disorders and Schizophrenia (SADS). Several biopsychiatric tests were run during the same week of investigation. Results indicate low levels of CSF somatostatin to be a state marker for episodes of depression characterized by sad appearance, feelings of tiredness, insomnia, and subjective inability to acknowledge any external precipitants for the depression. CSF somatostatin was negatively related to platelet monoamine oxidase (MAO) activity; MAO activity appeared to account better for the degree of melancholic features than did somatostatin. The ratio between 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) in CSF also correlated negatively with somatostatin. A positive relationship was noted between CSF xanthine and somatostatin. There was a highly significant curvilinear correlation between CSF somatostatin and serum TSH concentrations, but no correlations between CSF somatostatin and serum GH or prolactin, or with plasma cortisol before or after dexamethasone.
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PMID:Low levels of somatostatin in human CSF mark depressive episodes. 614 88


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