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)

Beta-adrenoceptor-mediated cyclic AMP formation was found to be increased in leukocytes from manic-depressive patients during untreated depression when compared with euthymic patients treated with antidepressants. The difference was dependent on the stimulation used (isoprenaline or a combination of noradrenaline and phentolamine) and was only significant when the combination was used. Histamine-stimulated cyclic AMP formation in leukocytes was enhanced in patients with untreated depression, both when compared with euthymic patients suffering from manic-depressive illness, with or without treatment with antidepressant drugs, and also when compared with control persons without any known psychiatric disease. Although at variance with the results of some other studies on the same topic, the results of the present study indicate that changes in receptor function in leukocytes may be a state-dependent marker in depressive illness.
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PMID:Enhanced histamine- and beta-adrenoceptor-mediated cyclic AMP formation in leukocytes from patients with endogenous depression. 282 89

In the cerebral ganglion of Aplysia californica synaptic transmission between identified neurones undergoes a prolonged decrease of efficacy following activation of a separate afferent pathway. Synaptic efficacy was measured as the amplitude of a monosynaptic and unitary excitatory response (test excitatory postsynaptic potential = test EPSP) generated by intracellular presynaptic stimulation. Test EPSP depression occurs with a delay of about 20 s, and may have a total duration of several minutes. Test EPSP depression is associated with a hyperpolarization of the presynaptic neurone. It is concluded that the test EPSP depression is due to presynaptic inhibition. Histamine mimics the pre- and postsynaptic effects obtained with activation of secondary afferent pathways.
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PMID:Presynaptic inhibition and histamine in cerebral ganglion of Aplysia. 285 30

Dissociation constants and receptor reserves for histamine acting at H2 receptors in guinea-pig right atria and papillary muscles were measured using the irreversible H2 receptor antagonist L-643,441. Histamine alone was less potent in papillary muscles than in right atria, and maximum responses of papillary muscles to histamine were more susceptible to depression by L-643,441 than were maximum responses of right atria. However, dissociation constants (-log KA values) for histamine calculated using 3 different doses of L-643,441 were 0.5 log unit greater in papillary muscles than in right atria. A more marked difference was found in the estimates of receptor reserve for histamine, which appeared to be much greater in right atria than papillary muscles.
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PMID:Irreversible antagonism of histamine H2 receptors in guinea-pig myocardium. 287 36

We have previously demonstrated a depression of airway H2-receptor function in sheep allergic to Ascaris suum antigen. To investigate whether this is a generalized defect, we studied the H1- and H2- histamine receptor functions in the pulmonary and systemic circulations of allergic and nonallergic sheep. Pulmonary arterial pressure, and cardiac output were measured for calculation of pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) before and immediately after a rapid intrapulmonary infusion of histamine (10 micrograms/kg), with and without pretreatment with H1- (chlorpheniramine) and H2- (metiamide) antagonists. Histamine alone increased mean PVR to 435 and 401% of base line and decreased mean SVR by 51 and 54% in the nonallergic and allergic sheep, respectively (P less than 0.001). In the nonallergic sheep following pretreatment with chlorpheniramine (selective H2 stimulation) or metiamide (selective H1 stimulation), histamine decreased SVR by 18 and 36%, respectively, suggesting that approximately two-thirds of the vasodepressor response was mediated by H1-receptors and one-third by H2-receptors. Combined H1- and H2-antagonists completely blocked the histamine response. In allergic sheep the histamine-induced decrease in SVR was primarily mediated by H1-receptors, because the response was blocked by H1-antagonist, chlorpheniramine, and the H2-antagonist, metiamide, had no effect. In the pulmonary circulation selective H1-stimulation caused a similar increase in PVR in allergic (365%) and nonallergic sheep (424%), whereas selective H2-stimulation caused a significant decrease in PVR in the nonallergic group (14%) but not in the allergic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Suppression of pulmonary and systemic vascular histamine H2-receptors in allergic sheep. 300 27

The complex syndrome of protein-energy malnutrition (PEM) in weanling children, usually complicated by concurrent presence of numerous adverse environmental factors, is a chronic stressful situation which elicits a number of neuroendocrine and metabolic adjustments. Histidine metabolism is severely impaired in PEM in children and in experimental animals, and evidence from the latter indicate markedly increased body burden of histamine. The brain is the organ most prominently affected. Although data are still incomplete, histamine conforms with most criteria required of a neurotransmitter. Histamine interacts with other neuroregulatory substances in modulating many neuroendocrine and vegetative processes. Some of the prominent pathophysiological features associated with PEM in children such as increased circulating cortisol, defective thermoregulation, fluid/electrolyte imbalance, impaired immunity, reduced cardiac output with prolongation of systemic recirculation time, and apathy bordering on a clinical state of depression are consistent with the known effects of histamine as determined by neurochemical and neuropharmacological studies. It is suggested that studies of histamine status in human PEM, and the functional relationships between markedly elevated level of this amine with other neuroregulatory substances, will shed more light on the complex pathogenesis of the nutritional syndrome.
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PMID:Pathophysiological implications of increased brain burden of histamine in protein malnutrition. 310 36

The symptom of carbohydrate craving and increased appetite (CHH) was studied in 180 outpatients receiving antidepressant treatment. One hundred and fifty-eight of these patients had a DSM-III diagnosis of panic disorder and 17, major depression. The incidence of CHH was similar in both diagnostic groups. Thus, antidepressant treatment is associated with CHH in patients with diagnoses, other than depression. Desipramine was least likely to induce CHH compared to imipramine, amitriptyline and doxepin. Most patients who developed CHH on imipramine no longer experienced this side effect when switched to desipramine. CHH was not more frequent among women and not associated with antidepressant dosage or treatment response. Histamine H-1 receptor blockade may be an important factor in the etiology of CHH.
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PMID:Carbohydrate craving and increased appetite associated with antidepressant therapy. 319 15

We studied the respiratory effects of cigarette smoke, 5% histamine aerosol, and dust in unanesthetized 1- to 7-day-old rabbits in a body plethysmograph. Cigarette smoke immediately provoked the animal's arousal and irregular breathing. Histamine and dust had no effect in some of the youngest animals. In others, 5-15 s from the onset of the exposure to either of the two stimuli, respiratory rate increased and the depth of breathing decreased. These changes were more pronounced with age. The fact that effects of dust and aerosol lessened with time of exposure showed adaptation to the stimuli. The age dependence of the reflex response was also observed after injection of 50 micrograms of histamine per kilogram into the external jugular vein in anesthetized (50 mg ketamine + 3 mg acepromazine per kg) and tracheostomized rabbits during the 1st wk of life. In 1-day-old animals, a short-lasting excitation was followed by apnea or a prolongation of expiratory phase. Peak amplitude of the diaphragmatic EMG (EMGdi) increased in all animals, but only in the youngest was the EMGdi increase paralleled by an increase in tidal volume. In vagotomized animals or animals pretreated with H1-blocker, histamine never affected timing parameters in animals greater than 1 day old. In the youngest animals, respiratory depression due to histamine was not abolished after vagotomy or promethazine. The results imply that inputs from the upper airways and the rapidly adapting pulmonary mechanoreceptors exert their effects on the pattern of breathing immediately after birth in rabbits. The importance of those inputs increases with maturation.
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PMID:Respiratory effects of cigarette smoke, dust, and histamine in newborn rabbits. 337 41

The histaminergic effect on electrically induced contractions and tritium release was studied in vitro, using strips from the wall of mature bovine ovarian follicles. Follicular fluid and blood plasma from the animals were analysed for electrolyte, bicarbonate, glucose and total protein concentrations in order to compare them with the concentrations of these components in the Krebs-Ringer solution used in the experiments. Electrical field stimulation (EFS) of the follicle strip caused a contraction which was completely blocked by tetrodotoxin and was predominantly of adrenergic origin since phentolamine, in contrast to atropine, blocked the response. The neurogenic response was inhibited by histamine in a concentration-dependent way via the H1-receptor since the H1-antagonist, pyrilamine, counteracted the inhibitory effect of histamine while the H2-antagonist, cimetidine, potentiated the effect. This histaminergic response of EFS-induced contractions could be reproduced in experiments where the H1-agonist, 2-methylhistamine, was inhibitory while the H2-agonist, 4-methylhistamine, had no obvious influence on the twitch response. Histamine reduced the contractile response to exogenous noradrenaline via the H1-receptor, because pyrilamine counteracted, and cimetidine potentiated the effect. The histamine-induced depression of the motor response to EFS and exogenous noradrenaline was probably due to a postjunctional effect mediated by the H1-receptor. Experiments utilizing [3H]noradrenaline release during EFS did not suggest prejunctional effects of histamine. Chemical determinations on follicle fluid and plasma showed that the artificial follicular fluid imitated well the environmental conditions the follicle wall is exposed to in situ.
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PMID:Alteration by histamine of the sympathetic nerve-mediated contractions in the bovine ovarian follicle wall in vitro. 356 22

The effects of bolus and infusion of ciramadol, dezocine, morphine and pentazocine were examined in anesthetized dogs. Cardiopulmonary parameters, blood PCO2, PO2 and pH and plasma histamine determinations were made. Ciramadol (2 and 8 mg/kg) did not exhibit any major activity. Dezocine produced slight respiratory depression at 2 mg/kg but no cardiopulmonary effects were observed at this dose. At 8 mg/kg there were also reductions in pulmonary compliance (Cdyn) and resistance (RL), tidal volume (VT) and a marked arterial hypotension. Morphine (2 mg/kg) elicited significant effects on all parameters examined: marked bronchoconstriction, increased arterial PCO2 and pH and corresponding decrease in PO2, slight increase in heart rate and dramatic arterial hypotension. Morphine was the only agent studied to elevate plasma histamine. Histamine (0.015 mg/kg) mimicked the cardiopulmonary actions of morphine but was virtually devoid of effect on blood gases and pH. Pentazocine (8 mg/kg) did not produce bronchoconstriction but did increase VT and reduce respiratory frequency. It produced increases in arterial PCO2 and reductions in pH and PO2. There was a slight bradycardia and hypotension within this dose. These results demonstrate that both ciramadol and dezocine possess less potential than either morphine or pentazocine for producing bronchoconstriction, respiratory depression, hypotension and histamine release.
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PMID:A comparison of the cardiorespiratory effects of ciramadol, dezocine, morphine and pentazocine in the anesthetized dog. 611 23

We investigated the effects of histamine applied by microiontophoresis onto serotonin-containing (serotonergic) cells recorded extracellularly in the dorsal raphe nucleus of the rat. Application of histamine at low iontophoretic currents (1-5 nA) produced a rapid depression of the firing of all serotonergic neurons tested. The H1-receptor antagonists mepyramine and diphenhydramine were unable to attenuate the histamine-induced response. Antagonism of the effect of histamine by the iontophoretic application of the H2-receptor antagonists cimetidine and metiamide was not possible to evaluate since both were found to exert potent inhibitory effects by themselves. In contrast, the nonimidazole-derived H2-receptor antagonist ranitidine, which had no effect by itself, selectively antagonized the histamine-induced depression of neuronal activity. Histidine, 3-methylhistamine and a variety of histamine agonists selective for H1- or H2-receptors were unable to mimic the effect of histamine in dorsal raphe. Histamine's effects may, in part, be mediated at a gamma-aminobutyric acid receptor complex as the gamma-aminobutyric acid antagonists bicuculline and picrotoxin rapidly and reversibly antagonized both the histamine- and the cimetidine-induced depression of serotonin cell firing; the glycine antagonist strychnine selectively blocked the inhibitory effect of glycine without altering the histamine-induced response. These data show an inhibitory effect of histamine on serotonin-containing neurons in the dorsal raphe; this effect may be partially mediated at a subtype of H2-receptor. These data further indicate that the inhibitory effects of histamine and cimetidine observed in the dorsal raphe nucleus may result, in part, from an action directly or indirectly at a gamma-aminobutyric acid receptor complex.
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PMID:Effects of histamine, H1- and H2-receptor antagonists on the activity of serotonergic neurons in the dorsal raphe nucleus. 613 28


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