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)

Effects of antidepressant drugs on the amygdaloid after-discharge induced by stimulating the amygdala in rats implanted with chronic electrodes, were investigated in correlation with anti-muricidal effects as well as neurotoxicity. Tricyclic antidepressants such as amitriptyline, imipramine and nortriptyline markedly depressed both after-discharge and muricide at doses smaller than neurotoxic doses. The effect of PF-257 was also the same as tricyclic antidepressants. On the other hand, methamphetamine and pipradrol blocked the muricide at doses smaller than neurotoxic doses without depressing the amygdaloid after-discharge. Major tranquilizers, chlorpromazine and clozapine depressed both after-discharge and muricide only at doses larger than those which impaired rotarod performance. Haloperidol, on the contrary, depressed the after-discharge without selectively blocking the muricide. Minor tranquilizers, diazepam and chlordiazepoxide did not block the muricide at doses smaller than neurotoxic doses, although they showed a marked depression of the after-discharge.
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PMID:Effects of antidepressant drugs on amygdaloid after-discharge in rats. 0 61

Morphine elicits dose-dependent tail erection in mice. Pretreatment of mice with atropine, phenoxybenzamine, propranolol, diphenhydramine, cyproheptadine or parachlorophenylalanine did not interfere with tail erection induced by morphone. Several neuroleptic drugs which are dopamine receptor blocking agents showed a clear antagonistic effect on morphine-induced tail erection (MITE). Haloperidol and penfluridol blocked MITE at doses which only produced a slight behavioral depression. Pimozide and chlorpromazine were less antagonistic than haloperidol and penfluridol and inhibited MITE only at doses which produced a marked behavioral depression. Results indicated that dopamine might be involved in tail erection induced by morphine. MITE in mice might be a useful model for the evaluation of neuroleptic drugs.
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PMID:Effects of neuroleptics on morphine-induced tail erection in mice. 2 20

The actions of various doses of haloperidol, pimozide, clozapine, and phenoxybenzamine were assessed on a conditioned-avoidance response (CAR) in control and 6-hydroxydopamine-treated rats, using a pole-climbing device. Haloperidol proved to be the most potent in disrupting the CAR. Pimozide was about 1.6 times less potent, and clozapine and phenoxybenzamine were approximately 52 and 155 times less potent than haloperidol, respectively. Prior treatment with 6-hydroxydopamine slightly enhanced the sensitivity to some of the doses of the DA and NE antagonists. Significantly lower levels of responding, however, were observed only after the highest dose of primozide. Clonidine was not only ineffective in reverting avoidance decrements, but also induced a further decline of the CAR. Apomorphine produced a partial, but significant, reversal of the haloperidol and pimozide-induced depression of conditioned responses. Regarding the clozapine-pretreated animals, a significant antagonism was observed only with the smaller dose of apomorphine. The highest dose induced a further decline of the CAR. The DA agonist was also ineffective in the phenoxybenzamine-injected rats. Amphetamine was effective in antagonizing the avoidance decrements produced by all the CA antagonists. Our results support the suggestion that CAR depends on both DA and NE mechanisms. DA seems to be more significant that NE, however, since the CAR was more depressed when receptors depending on the former neurotransmitter were blocked.
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PMID:The actions of dopaminergic and noradrenergic antagonists on conditioned avoidance responses in intact and 6-hydroxydopamine-treated rats. 10 52

Six patients with a family history of Huntington's chorea (HC) participated in a double blind crossover trial involving four treatments--lithium carbonate, haloperidol, lithium carbonate and haloperidol, and placebo. Each treatment was administered for three weeks and, at the end of each treatment period, assessments were made of chorea and a number of psychological variables. None of the treatments significantly affected chorea measurements. With regard to the psychological variables, the levels of irritability, the frequency of angry outbursts and depression did appear to be affected in some patients by the treatment. Three patients improved on a combination of lithium carbonate and haloperidol while the remaining three did not. Haloperidol alone significantly raised depression ratings above levels for other treatments including placebo. It is suggested that lithium carbonate and haloperidol together should be seriously considered in the treatment of HC when patients are excessively irritable and impulsive.
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PMID:A double blind trial of lithium carbonate and haloperidol in Huntington's chorea. 12 78

Hyperactivity produced in mice with morphine or fentanyl, and methylamphetamine was antagonized by naloxone. The depression of locomotor activity induced by codeine was practically unchanged by the opiate antagonist. L-DOPA did not restore the stimulatory action of morphine and fentanyl in reserpinized mice. The hyperactivity produced by morphine and fentanyl was abolished in mice treated with alpha-methyl-p-tyrosine, but this was restored by L-DOPA administration. Agents inhibiting the central noradrenaline receptors, phentolamine, phenoxybenzamine, and aceperone, prevented or even reversed the locomotor stimulatory action of morphine and fentanyl. Pimozide did not affect the increase of locomotor activity produced by morphine, but depressed that induced by fentanyl. Haloperidol, used in a dose which did not affect the locomotor activity of mice, completely blocked or even reversed the stimulatory action of morphine and fentanyl, and potentiated the depression of locomotor activity produced by pentazocine and codeine. Diethyldithiocarbamate significantly depressed, but did not inhibit completely the stimulatory action of morphine and fetanyl. The stimulatory action of methylamphetamine was also significantly depressed. It seems that the stimulatory effect of morphine and fentanyl depends on the release of endogenous noradrenaline.
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PMID:Central action of narcotic analgesics. Part III. The role of endogenous noradrenaline in hyperactivity induced by morphine or fentanyl in mice. 21 79

It was found that spiperone and pimozide in doses which themselves do not influence the flexor reflex of the hind limb of the spinal rat inhibit stimulation of this reflex induced by serotoninomimetic drugs (LSD and fenfluramine). Higher doses of spiperone depress the flexor reflex and inhibit the stimulating effect of clonidine. Pimozide has no such effect. Haloperidol in doses which do not influence the action of LSD and fenfluramine produces a depression of the flexor reflex and antagonizes the action of clonidine. Our findings indicate that, irrespective of their antidopamine action, spiperone has a central antiserotonin effect and an antinoradrenaline one, pimozide--an antiserotonin one and haloperidol--an antinoradrenaline one.
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PMID:The effect of haloperidol, spiperone and pimozide on the flexor reflex of the hind limb of the spinal rat. 73 Dec 32

Mice, administered haloperidol 3 mg/kg/day, in their drinking water for 21 days, were tested for their responsiveness to cholinergic and anticholinergic drugs 4 days after withdrawal from haloperidol (or vehicle). Haloperidol-treated animals administered methylhyoscine (1 mg/kg i.p.) and various doses of physostigmine (5 to 1215 microgram/kg) displayed significantly less depression of locomotor activity than vehicle-treated animals. Atropine, 5 mg/kg, whilst ineffective in producing locomotor stimulation in vehicle-treated animals, produced marked stimulation in haloperidol-treated animals. Methylatropine (5 mg/kg) did not produce significant stimulation in either group. Dopamine receptor supersensitivity was present in these animals as haloperidol-treated mice, pretreated with alpha-methyltyrosine and reserpine, displayed a significantly greater locomotor response to apomorphine than did vehicle-treated animals. The data support the hypothesis that long-term administration of haloperidol produces an apparent hyposensitivity of central muscarinic receptors.
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PMID:The demonstration of a change in responsiveness of mice to physostigmine and atropine after withdrawal from long-term haloperidol pretreatment. 87 70

Administration of 0.025--0.1 mg/kg of apomorphine i.p. to mice produced a dose-dependent locomotor depression. Haloperidol, 0.025 mg/kg, produced locomotor stimulation, whereas 0.1 mg/kg caused locomotor depression. Pretreatment with haloperidol also reversed the depression caused by apomorphine. The functional antagonism is discussed in terms of a possible agonist-antagonist interaction on dopaminergic autoreceptors.
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PMID:Antagonism by haloperidol of locomotor depression induced by small doses of apomorphine. 87 71

1. The positive chronotropic and inotropic actions of dopamine and noradrenaline have been compared in anaesthetized dogs and isolated guinea-pig atria. 2. Inotropic activity was measured with a strain-gauge arch in vagotomized dogs or estimated from max (dp/dt) in dogs with denervated hearts. 3. The effects of propranolol and haloperidol on the concentration-response curves to both amines were studied in isolated atria. 4. In anaesthetized vagotomized dogs noradrenaline was more potent than dopamine but dopamine appeared to have a selective inotropic action, less apparent with noradrenaline. In denervated hearts, doses of noradrenaline and dopamine which caused similar increases in max (dp/dt) also caused similar increases in heart rate. 5. In isolated atrial preparations, concentrations of dopamine and noradrenaline which produced similar increases in force of contraction also had similar chronotropic effects. 6. Propranolol produced a shift to the right of the concentration-response curves to both dopamine and noradrenaline but the antagonism of noradrenaline was quantitatively greater. Haloperidol had not effct in concentrations below those found to cause general tissue depression. 7. It is concluded that neither dopamine nor noradrenaline show any real difference in their relative inotropic and chronotropic activities in the absence of autonomic innervation.
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PMID:A comparison of the cardiac actions of dopamine and noradrenaline in anaesthetized dogs and guinea-pig atria. 88 5

To ascertain whether neuroleptics act on the caudate nucleus itself, the effects of these compounds as well as other centrally acting drugs were examined in relation to caudate spindle and EEG arousal responses (sciatic nerve stimulation) in gallamine-immobilized cats. Haloperidol and chlorpromazine enhanced the caudate spindle at a dose which had no effect on the EEG arousal response. On the other hand, clozapine and a higher dose of chlorpromazine enhanced the caudate spindle, but depressed the arousal response. High frequency stimulation of the sciatic nerve suppressed the caudate spindle. Pentobarbital, biperiden and diazepam, while depressing the arousal response, caused an enhancement of the caudate spindle. Imipramine at a low dose had no effect on either response, whereas at a high dose this drug enhanced the caudate spindle with concomitant depression of the arousal response. From these results, it may be concluded that the enhancing action on the caudate spindle induced by haloperidol and a low dose of chlorpromazine is due to an increase in susceptibility of the caudate nucleus itself. In addition, it is suggested that depression of the activating system is involved in an appearance of the caudate spindle.
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PMID:Effect of psychotropic drugs on caudate spindle in cats. 100 8


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