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)

We used the electric organ of Torpedo, a modified neuromuscular system, to investigate the direct effects of antipsychotic drugs on cholinergic transmission. All the antipsychotic drugs tested inhibited transmission by decreasing the amount of ACh released by nerve impulses. Their potency for this action was as follows: trifluoperazine less than clozapine less than thiethylperazine less than droperidol less than haloperidol less than chlorpromazine = beta-flupentixol less than alpha-flupentixol. Depression of ACh release by antipsychotics was poorly reversible, and was not mediated by dopamine receptors in this system since neither dopamine nor apomorphine had any effect on transmission. Antipsychotics did not act through presynaptic cholinergic receptors since the effect was not antagonized by atropine or quinuclidinyl benzilate. Trifluoperazine had no effect on the total ACh content of the tissue, on the compartmentation of ACh inside and outside synaptic vesicles, or on the rate of ACh turnover or the accumulation of 45Ca observed after repetitive stimulation. We conclude that antipsychotic drugs depress the neurally evoked release of ACh by acting directly on the releasing mechanism.
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PMID:Antipsychotic drugs depress acetylcholine release in the Torpedo electric organ, a purely cholinergic system. 286 52

We observed changes in the performance of isolated right ventricle strips taken from rats when calcium was repleted following various periods of calcium depletion in order to study certain phenomena, such as the calcium paradox, in this preparation. Furthermore, to assess the possible role of calmodulin in this myocardial damage, the effects of known calmodulin inhibitors such as trifluoperazine and chlorpromazine on the contractility and resting tension were studied by means of the calcium repletion after a calcium-depleted period of 12 min. The temperature was kept at 37 degrees C, and the muscle strips were stimulated electrically at a rate of 0.25 Hz. When there was a calcium-depleted period of longer than 8 min, a marked increase in resting tension was observed and reached maximum at 2 to 4 min. The recovery of peak developed tension and peak positive or negative dT/dt worsened as the duration of the calcium depletion was longer. These findings indicate the massive intracellular calcium influx by the calcium reintroduction and the myocardial damage induced by the calcium overload as observed in isolated whole hearts. Treatment with trifluoperazine (1-5 microM) and chlorpromazine (1-5 microM) did not inhibit a rise in resting tension significantly after the calcium repletion, except for 5 microM of both drugs at 6 min. Trifluoperazine significantly improved the recovery of the contractility (developed tension and dT/dt), whereas the protective effect of chlorpromazine was not obtained. These results suggest that the depression of calmodulin activity is beneficial in the prevention of myocardial damage produced by calcium repletion, although there is a difference in the effect of the calmodulin inhibitors, trifluoperazine and chlorpromazine.
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PMID:Effects of trifluoperazine and chlorpromazine on calcium-repleted injury in isolated ventricle strips. 407 89

Chlorpromazine (ClP) and trifluoperazine (TFP) depress electrical and mechanical activity of ureter smooth muscle cells. Contraction was depressed by less doses of the substances applied as compared with the processes responsible for generation of spike activity. ClP causes the displacement of the dose-effect curve for Ca2+ towards larger concentrations of the latter. Trifluoperazine displaces the dose-effect curve for contraction to the right and downwards. It is concluded that inhibition of contraction and depression of ClP and TFP spikes is due to the calmodulin blocking on which kinase activity of myosin light chains depends. It is supposed that processes responsible for activation of the membrane systems of Ca2+ transport in the process of spike generation are also calmodulin-dependent.
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PMID:[Study of electromechanical coupling in smooth muscle cells of the ureter using phenothiazines]. 672 4

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

Background: Patients with mental disorders, such as depression and anxiety, who seek medical care in private psychiatric clinics in Riyadh, Saudi Arabia, have recently expressed concerns to doctors about difficulty in filling psychotropic medications, such as Amitriptyline and Aripiprazole, at retail community pharmacies. Objectives: The aim of this study was to investigate whether there is a shortage of some commonly prescribed psychotropic medications in retail community pharmacies in Saudi Arabia, and if so, to explore the possible reasons behind the shortage of these medications. Methods: The availability of 28 commonly prescribed psychotropic medications was checked in multiple retail community pharmacies in 4 different regions of Saudi Arabia. Further, potential reasons behind the shortage of some psychotropic medications in retail community pharmacies were also explored. Results: Amitriptyline, Amoxapine, Aripiprazole, Bupropion, Buspirone, Duloxetine, Haloperidol, Hydroxyzine, Lithium, Prochlorperazine, Procyclidine, Promethazine, Thioridazine, Trazodone, and Trifluoperazine were unavailable in over half of the 248 community pharmacies surveyed. Four possible reasons behind the shortage of these medications were reported by 31 pharmacists working in different retail community pharmacies' purchasing departments, with a majority (58.06%) reporting the primary reason for a shortage of these medications that they are slow-moving items with low profit margins. Conclusions: The findings of this study should expedite the reform process in both the Ministry of Health and the Saudi Food and Drug Authority (SFDA) to publish and enforce an essential list of medications for retail community pharmacies, which should include the most commonly prescribed psychotropic medications.
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PMID:Shortage of psychotropic medications in community pharmacies in Saudi Arabia: Causes and solutions. 2872 47