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)

Involvement of the cholinergic and catecholaminergic mechanisms in the caudate spindle recorded from the anterior and posterior sigmoid gyri was examined in cats. Physostigmine (0.01 to 0.1 mg/kg i.v.) abolished the appearance of the caudate spindle. These inhibitory effects were antagonized by the administration of atropine (0.25 to 1 mg/kg i.v.). The caudate spindle was inhibited by high frequency stimulation of the mesencephalic reticular formation: This inhibitory effect was antagonized by atropine. On the other hand, L-DOPA (25 to 50 mg/kg, i.v.), L-DOPA + MAO inhibitor and methamphetamine (0.5 to 5 mg/kg i.v.) did not influence the caudate spindle. These results suggest an involvement of cholinergic mechanism in depression of the caudate spindle.
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PMID:Involvement of the cholinergic mechanism in depression of the caudate spindle. 53 59

Investigation has been made into the processes regulating the function activity of rat brain 5-hydroxytryptamine (5-HT) and the way that drugs used to treat depression act on these processes. Use was made of both biochemical measurements and a behavioural model in which the hyperactivity which follows increased 5-HT synthesis and release was measured as an index of functional activity of the amine. The following mechanisms are suggested to be important in the control of 5-HT function. Presynaptic mechanisms; precursor availability and the transport of tryptophan across the neuronal membrane, intraneuronal metabolism by monoamine oxidase, compartmentation, release and re-uptake. Postsynaptic mechanisms; the sensitivity of the post-synaptic receptor, the role of peptides in altering the size of the post-synaptic response and the action of other neurotransmitters controlling the magnitude of the postsynaptic response. In this regard 5-HT function has been shown to be altered by both dopamine and GABA. The action of anti-depressant drugs on these mechanisms is discussed.
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PMID:Processes regulating the functional activity of brain 5-hydroxytryptamine: results of animal experimentation and their relevance to the understanding and treatment of depression. 56 59

Intraventricular administration of serotonin to rats causes 'wet-dog' shakes, a sign of morphine withdrawal. The frequency of shakes is dose-dependent. Shaking is potentiated by pretreatment with an inhibitor of monoamine oxidase or with 5,7-dihydroxytryptamine, and is depressed by morphine or serotonin receptor blockers. Depression of serotonin-induced shaking by morphine is reversed rapidly by naloxone. However, naloxone did not reverse the inhibition of 'wet-dog' shakes caused by serotonin receptor blockers.
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PMID:Effect of morphine on 'wet-dog' shakes caused by cerebroventricular injection of serotonin. 57 8

The influence of 5-hydroxytryptamine (5-HT) on the activity of the respiratory and vasomotor centers was studied by injecting 5-HT into the lateral and fourth ventricles of lightly anaesthetized cats. 50 and 500 mu g of 5-HT injected into the lateral ventricle induced a shortlasting increase in frequency and/or tidal volume followed by a prolonged and dose-dependent reduction of frequency, tidal volume and minute volume, concurrent with an increase in end expiratory CO2. The CO2 responsiveness of the respiratory center was depressed and the blood pressure levels were also lowered. All these effects were markedly enhanced by monoamine oxidase inhibition with i.v. tranylcypromine injected 75 min prior to 5-HT. 50 mu g of 5-HT injected into the fourth ventricle induced a depression of respiration similar to that observed in the lateral ventricle studies, with the exception that the early stimulation was abolished.
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PMID:Inhibition of the activity of the respiratory and vasomotor centers by centrally administered 5-hydroxytryptamine in cats. 58 27

The multiple manifestations of depression may mimic those associated with many physical illnesses, leading to delay in diagnosis. The consequences of depression are disability, suffering, and sometimes death by suicide. Antidepressant drugs have greatly improved the prognosis for the depressed patient. Tricyclics are the drugs of first choice, with monoamine oxidase inhibitors playing a secondary role except in special instances. Drugs can be used along with electroconvulsive therapy when treatment is urgent. Differences in the pharmacologic effects of tricyclics may affect their choice for individual patients. Monitoring of plasma concentrations of tricyclics may uncover some sources of drug failure, such as altered drug kinetics in an individual patient or noncompliance with treatment. Side-effects of antidepressant drugs are numerous; most represent extensions of known pharmacologic actions. Overdoses produce severe intoxications that require expert and assiduous management.
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PMID:Treatment of Depression with drugs. 66 96

Combined monoamine oxidase (MAO) inhibitor-tricyclic antidepressant therapy and electroconvulsive therapy (ECT) were compared in a population of refractory depressive patients. Seventeen patients were randomly assigned to either of the treatment groups, and an independent observer was used to rate overall progress. Between four and ten ECTs or a combination of phenelzine and amitriptyline were administered. Assays for MAO activity and plasma levels of amitriptyline and nortriptyline were performed. In both psychotic and neurotic depression, ECT was superior. When depression was accompanied by character disorder, the response was generally poor. Adequate levels of MAO inhibition were obtained, but tricyclic antidepressant levels were low. Electroconvulsive therapy is still considered to be the treatment of choice for severe depression, whereas the combination of low doses of phenelzine and amitriptyline are ineffective. This treatment modality needs further investigation.
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PMID:A comparison of electroconvulsive therapy and combined phenelzine-amitriptyline in refractory depression. 72 3

In a double-blind, controlled experiment, 62 outpatients with symptoms of depression with anxiety were selected for treatment with phenelzine sulfate, 60 mg daily, phenelzine sulfate, 30 mg daily, or placebo for six weeks. Forty-nine patients (79%) completed the experiment. Phenelzine sulfate, 60 mg daily, was significantly more effective than placebo in relieving symptoms of both depression and anxiety. Phenelzine sulfate, 30 mg daily, did not differ from the placebo. Only phenelzine sulfate, 60 mg daily, resulted in a median inhibition of platelet monoamine oxidase that exceded 80%. The results confirm a previous study that found phenelzine to be effective in the treatment of outpatients with depressive-anxiety states. Drug dosage is an important variable influencing clinical outcome in this patient group.
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PMID:A multiple-dose, controlled study of phenelzine in depression-anxiety states. 76 25

The treatment of obesity is one of the major measures available today in the field of preventive medicine. In particular, the coronary epidemic of Western civilisation would be halted, and most cases of maturity-onset diabetes prevented, if obesity were to be treated effectively. Anorectic drugs act mainly on the satiety centre in the hypothalamus to produce anorexia. They also have various metabolic effects involving fat and carbohydrate metabolism, but many of these may be secondary to loss of weight. Most of the drugs are related directly or indirectly to amphetamine and in addition act by increasing general physical activity. Anorectic drugs tend to lose their effect after some months, and part of this reduction in effect may be due to chemical alterations produced by the drugs in the brain. All the drugs, with the exception of fenfluramine, have a stimulant effect on the central nervous system in some individuals, resulting in restlessness and nervousness, irritability and insomnia. Fenfluramine commonly produces drowsiness in normal doses, but has stimulant effects with overdosage. Dexamphetamine, phenmetrazine and benzphetamine all tend to cause euphoria and the risk of addiction is therefore considerable. Euphoria occasionally occurs with diethylpropion, phentermine and chlorphentermine, but to a much lesser extent. Side-effects also occur due to sympathetic stimulation and gastro-intestinal irritation. These side-effects may cause some individuals to stop taking the drug, but are never serious or dangerous. Drug interactions may occur with monoamine oxidase inhibitors and to a clinically unimportant extent, with antihypertensive drugs. The anorectic drugs have a very definite part to play in the treatment of obesity, mainly for those individuals who have altered their eating habits but have come to a plateau of weight which they find difficult to get below. The drugs are best given in a long-acting form and can safely be continued as long as weight loss persists, provided that the clinician exercises careful supervision. Dexamphetamine, phenmetrazine and benzphetamine should rarely be used because of the danger of addiction, and chlorphentermine is potentially hazardous for long-term use. Diethylpropion emerges as the drug of first choice, as fenfluramine has a tendency to cause depression and has a higher incidence of side-effects. Fenfluramine is mainly useful for people who are especially tense and for obese maturity-onset diabetics who have been unable to lose weight with the biguanides. Mazindol and phentermine appear to be useful as alternative drugs.
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PMID:Anorectic drugs: use in general practice. 78 35

The effect of nomifensin (Hoechst 36984), a synthetic psychotropic drug whose structure differs from MAO inhibitors and tricyclics, was studied in a double blind comparative trial with desimipramine in patients with various depressive syndromes. Forty-three patients (23 in the nomifensin group and 20 in the desimipramine group) were studied for 6 weeks. Clinical follow-up was done with the Wittenborn scale (WPRS), Hamilton's rating scale for depression (HRS), Zung's scale (SDS), and the PEN inventory. The average daily dose was nomifensin 84 mg and desimipramine 76 mg. Changes in HRS, WPRS and SDS showed statistically significant improvement with both treatments. A moderate anxiolytic effect was found in the nomifensin group, whereas medication had to be discontinued in two desimipramine-treated patients because of its drive-enhancing effect. Urinary phenylethylamine excretion rose in 2 out of 8 patients after 5 weeks of treatment with nomifensin.
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PMID:A double blind comparative trial of nomifensin and desimipramine in depression. Relationship between treatment and phenylethylamine excretion. 78 70

Platelet MAO activity decreased by 40% (p less than .001) in a group of 11 male patients with primary depression after 3 weeks of treatment with either amitriptyline or imipramine. This finding, together with data from previous in vitro studies demonstrating tricyclic-induced inhibition of mitochondrial MAO, suggests that inhibition of MAO plays a role in the clinical action of tricyclic antidepressant drugs.
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PMID:In vivo inhibition of platelet MAO activity by tricyclic antidepressants. 83 43


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