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)

To determine the role of central serotonergic systems in modulating the cough reflex, the effects of serotonergic agonists on the respiration and the cough reflex were comparatively studied. Male and female cats were anesthetized with sodium pentobarbital. Respiration and cough reflex were measured using a pneumotachograph via a cannula inserted into the trachea. The cough reflex was elicited by electrical stimuli to the superior laryngeal nerve. Tranylcypromine, a MAO inhibitor, in a dose of 5 mg/kg, i.v., increased the respiration, but depressed the cough reflex. The serotonin precursor 5-hydroxytryptophan (5 mg/kg, i.v.) depressed the respiration and the cough reflex. Haloperidol (2 mg/kg, i.v.) abolished the tranylcypromine-stimulated respiratory responses, and it intensified the tranylcypromine induced cough depression. It is concluded that the increase in serotonin levels in the brain has a depressant influence on the central generating mechanisms of the cough reflex. Furthermore, central dopaminergic mechanisms seem to play a modulating role on the cough reflex.
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PMID:Involvement of central serotonergic mechanisms in the cough reflex. 349 20

In symptomatic patients with borderline disorder, we conducted a double-blind, placebo-controlled trial of haloperidol and amitriptyline hydrochloride to test the differential efficacy of medication against the affective and schizotypal symptoms that characterize the disorder. Sixty-one patients, diagnosed by the Diagnostic Interview for Borderline of Gunderson et al, completed randomized trials of haloperidol (n = 21), amitriptyline (n = 20), and placebo (n = 20). Medications were given in dose ranges of 4 to 16 mg for haloperidol (mean, 7.24 mg) and 100 to 175 mg for amitriptyline hydrochloride (mean, 147.62 mg) for five-week periods, with weekly self-rated and observer-rated measures of mood, schizotypal symptoms, and global functioning. Haloperidol was superior to both amitriptyline and placebo on a composite measure of overall symptom severity, with no difference between amitriptyline and placebo. Haloperidol produced significant improvement on a broad spectrum of symptom patterns, including depression, anxiety, hostility, paranoid ideation, and psychoticism. In contrast, amitriptyline was minimally effective, with small gains limited to some areas of depressive content. The magnitude of change tended to be modest and was more apparent in self-rated than observer-rated measures.
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PMID:Progress in pharmacotherapy of borderline disorders. A double-blind study of amitriptyline, haloperidol, and placebo. 352 32

The results of a standardized examination of 135 schizophrenics shows that the "depressive factor" is less pronounced during differential neuroleptic therapy (Clozapin, Haloperidol) and in the control group of schizophrenics receiving no drug treatment. This suggests that the depressive syndrome among schizophrenics is not manifested as a result of pharmaceutical action. The author proposes that neuroleptic therapy tailored to the patient can ameliorate the depressive syndrome observed in schizophrenics. Both psychoreactive and disease specific factors may play a role in the pathogenesis of depression among patients with this disease.
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PMID:[Depressive syndromes within the scope of schizophrenic diseases]. 357 44

As one index of sympathetic reactivity, electrodermal responses (EDR) were evoked from central (hypothalamic) and peripheral (ulnar nerve) sites in pentobarbital-anesthetized cats. When compared with intravenous chlorpromazine (ED50 approximately 1.0 mg/kg), only thioridazine, trifluoperazine, and pimozide were less potent than chlorpromazine in reducing the amplitude of these centrally-evoked sympathetic-cholinergic responses. Perphenazine and methotrimeprazine (a non-neuroleptic phenothiazine) were about twice as potent as chlorpromazine. Haloperidol and triflupromazine were about 5 times as potent and chlorprothixine was more than 10 times as potent. None of these agents reduced the peripherally-evoked electrodermal response, indicating a CNS mode of action. Diazepam was without effect at either site. In addition, pretreatment with yohimbine (0.5 mg/kg. i.v.) did not significantly alter the ED50 for any of the above drugs. These results demonstrate that all of the phenothiazines and non-phenothiazine neuroleptics tested produce a dose-dependent central sympatho-inhibition and that diazepam does not. The results also suggest that there is no significant correlation between central sympatho-inhibition and the antipsychotic potency of these compounds and that their depression of central sympathetic outflow is independent of alpha-adrenergic mechanisms in the CNS.
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PMID:A quantitative assessment of CNS sympatho-inhibition produced by psychotropic drugs. 612 1

The activity of neurones in the zona compacta of the rat substantia nigra was recorded extracellularly in vitro. Dopamine produced a dose-dependent depression of firing, threshold doses being in the 3 microM range. The inhibitory effects of dopamine were antagonized by (-)-sulpiride (pA2 7.5), haloperidol (pA2 8.4) and cis-flupenthixol (pA2 6.9). The actions of gamma-aminobutyric acid (GABA) were not affected by these compounds. The gradients of Schild plots of data for (-)-sulpiride were less than unity while those for haloperidol and cis-flupenthixol were greater than unity, which suggests that the antagonism was not competitive. This is discussed with regard to the use of a bioassay system in the analysis of the effects of antagonists. Haloperidol and (-)-sulpiride were found to have similar potencies, as dopamine receptor antagonists, to those predicted from biochemical and clinical efficacy studies, but cis-flupenthixol was less potent than expected.
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PMID:The actions of antipsychotic drugs on dopamine receptors in the rat substantia nigra. 614 43

Unilateral motor cortex injury in the cat results in a prolonged loss of tactile placing in the forelimb contralateral to the injury. Amphetamine (5 mg/kg) temporarily reverses this tactile placing deficit as early as 4 days following the injury. Racemic amphetamine was found to produce a significantly more prolonged restoration of placing than the d isomer, which was significantly more effective than the l isomer. Haloperidol (0.4 mg/kg) blocked the amphetamine-induced recovery of placing responses and also blocked placing in nondrugged cats showing partial spontaneous recovery. This dosage of haloperidol had no effect on tactile placing in normal cats. Apomorphine at moderate dosages (0.25 and 0.5 mg/kg) produced a weak restoration of tactile placing in motor cortex-injured animals. These pharmacological data suggest that the loss of tactile placing after motor cortex injury is due to a depression of catecholaminergic function, which is temporarily reversible by catecholaminergic stimulation.
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PMID:Amphetamine and apomorphine restore tactile placing after motor cortex injury in the cat. 640 67

The effects of trifluoperazine and haloperidol on protective activity of phenazepam were studied during seizures in mice treated with pentylenetetrazole (an index used for the appraisal of tranquilizing activity) as was their action on the phenazepam-induced depression of the test potential in the recovery cycles of somatosensory primary response. Trifluoperazine administered in doses of 0.1-0.5 mg/kg potentiated anticonvulsant action of phenazepam but did not change its effects on the recovery cycles of primary response. Haloperidol also potentiated anticonvulsant action of phenazepam. However, the doses administered were 4-5-fold lower than the tranquilizing doses of haloperidol. The drug also increased the depression of the test potential in the somatosensory recovery cycle, caused by phenazepam. This suggests an increment of GABA-positive effect of the tranquilizer. It appears that higher activity of haloperidol in elevating anticonvulsant and, probably, anxiolytic effects of phenazepam is determined by interaction of these drugs on the level of cortical GABA-ergic receptors.
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PMID:[Effect of triftazin and haloperidol on the activity of phenazepam]. 688 8

A 24-week double-blind study was conducted to compare haloperidol and thiothixene for efficacy and safety in 46 schizophrenic outpatients. In addition to the standard psychiatric rating scales, Brief Psychiatric Rating Scale (BPRS), Nurses' Observation Scale for Inpatient Evaluation (NOSIE), and Evaluation of Social Functioning Rating (ESFR), two scales more sensitive to the incidence of treatment emergent depression were utilized. They were the Hamilton Depression Scale (HPRSD) and the Zung Self-rating Depression Scale (ZUNG). On the BPRS factors, haloperidol was significantly superior to thiothixene in Thought Disturbance and Hostility-Suspiciousness, and in Total symptomatology. Haloperidol was also significantly superior to thiothixene in Cognitive Disturbance on the HPRSD. Results of global evaluations suggested haloperidol produced slightly more rapid relief of symptoms than did thiothixene. The inclusion of the depression scales was useful in following patients who exhibited depressive symptoms; clinically significant depression was seen in 5 patients receiving haloperidol and 3 receiving thiothixene. A high incidence of akathisia in the thiothixene group was responsible for a statistically significant difference between groups in the number of central nervous system symptoms. Mean doses of test drugs were 17.5 mg/day for haloperidol an 31.8 mg/day for thiothixene. The study showed that haloperidol was equal to and in some parameters superior to thiothixene in producing improvement in the symptoms of psychosis.
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PMID:Psychopharmacological correlates of post-psychotic depression: a double-blind investigation of haloperidol vs thiothixene in outpatient schizophrenia. 703 57

Haloperidol, a widely used neuroleptic, produced a significant depression of the rate of [3H]thymidine incorporation into the DNA of 11-day-old rat brain. The reduction of in-vivo DNA synthesis rate was detectable by 4 h after subcutaneous injection of a single dose of haloperidol (20 mg/kg) and through the period 10-24 h after drug treatment the rate was less than 50% of that of controls in the forebrain. [3H]Thymidine incorporation returned to control values by 32 h. The effect on the cerebellum was similar but less pronounced. The depression was dose-dependent and a half-maximal effect was produced with haloperidol doses of 5-10 mg/kg. Parallel histological studies on treated rats suggested prolongation of the DNA synthesis phase of the cell cycle in the forebrain subependymal layer, associated with an increase in turnover time of about 15%.
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PMID:Effects of haloperidol on cell proliferation in the early postnatal rat brain. 709 84

In the study the usefulness was assessed of haloperidol depot preparation in 50 mg ampoules produced by Warsaw Pharmaceutical Works POLFA in the treatment of schizophrenia. The study group comprised 30 patients, 12 females and 18 males, aged 18-70 years. Before haloperidol administration all other drugs were withdrawn. Haloperidol depot was injected intramuscularly after 7-10 days of oral administration of haloperidol. The injections were done at 3-week intervals during 26 weeks. The mean interval between the injections was 17.8 days, and the mean dose was 77.0 mg. The effectiveness of the drug was assessed using Overall scale (BPRS) measuring the intensity of 18 psychotic symptoms in the following weeks of the trial: 0, 1, 2, 3, 4, 7, 10, 13, 17, 20, 23 and 26. The depot haloperidol preparation (Decaldol) was studied assessing its effects on productive and defect symptoms and depression. The strongest effect was exerted on productive symptoms, less pronounced effect was on psychotic defects, and lowest on depression symptoms. Improvement of the psychosis was noted in 20 cases, deterioration in 8 and no change was observed in two patients. The present trial period was not completed by 19 patients, 6 due to psychotic deterioration, 5 patients had intense extrapyramidal adverse effects and in 2 cases worsening of mental condition was associated with adverse effects. In this subgroup of 19 patients 9 were improved, 8 were worse, and 2 had no change in relation to initial status. In the remaining 11 cases who completed the study only full of considerable improvement was found.
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PMID:[Evaluation of clinical usefulness of decaldol (haloperidol decanoate) produced by WZF Polfa in Warsaw in long-term treatment of schizophrenia]. 765 93


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