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PubMedDate not supplied

Haloperidol-induced changes in the regional cerebral pharmacokinetics of apomorphine.

Haloperidol did not change significantly the rate of penetration of apomorphine to three investigated structures of the rat brain: striatum, limbic forebrain and cerebellum. It depressed, however, significantly the accumulation of apomorphine in the striatum and limbic forebrain; in the cerebellum, in which the accumulation of apomorphine was very low, haloperidol did not change it. In haloperidol-pretreated rats the pattern of elimination of apomorphine from the striatum changed, revealing the presence of two compartments; this was not observed in the limbic forebrain, from which the elimination was linear, both in the presence and absence of haloperidol.

Animals↗

PubMed1977

Pre- and post-synaptic actions of apomorphine: differentiation by rotatory effects in normal rats.

Normal rats were tested for rotation (circling behavior) following d-amphetamine (1.0 mg/kg) and, a week later, following apomorphine (10.0 mg/kg). In most rats, d-amphetamine and apomorphine elicited rotation in opposite directions whereas, in some rats, the two drugs elicited rotation in the same direction. Subsequently, alpha-methyl-p-tyrosine was found to antagonize the rotatory effect of apomorphine in the latter but not in the former rats. The results suggest that apomorphine has both pre- and post-synaptic actions and that relative sensitivity to these actions varies among rats.

Animals↗

PubMed1978

Inhibition of apomorphine-induced behaviors by derivatives of 2-amino-1, 2, 3, 4-tetrahydronaphthalene.

In order to elucidate the pharmacological properties of a series of 1-phenyl-2-aminopropane and 2-amino-1, 2, 3, 4-tetrahydronaphthalene derivatives, their ability to inhibit a number of apomorphine-induced behaviors was investigated. Several members of the series under study were potent inhibitors of apomorphine-induced pecking behavior in pigeons, emesis in dogs, and gnawing in rats. In addition, these compounds were able to inhibit responding in self-stimulating rats and to a lesser degree counteracted the depression of the linguomandibular reflex induced by 5, 6-dihydroxy-2-dimethylamino-1, 2, 3, 4-tetrahydronaphthalene (M-7) in the cat. The most effective member of the experimental compounds was N-methyl-5, 8-dimethoxy-2-amino-1, 2, 3, 4-tetrahydronaphthalene; however, neither this material nor any of the related structures were able to inhibit apomorphine-induced rotational behavior in substantia nigra lesioned rats. The possibility that the more effective members of the experimental series are able to inhibit certain apomorphine-induced behaviors by stimulation of central alpha adrenergic receptors is discussed.

Animals↗

PubMed1983

Effects of pimozide and apomorphine on insulin secretion from the perfused rat pancreas.

The effects of apomorphine, a partial agonist of dopamine, and of pimozide, an agent commonly used as an antagonist of dopamine, on insulin secretion from the perfused rat pancreas were studied. Apomorphine (10 and 100 microM) significantly reduced the insulin released in response to a stimulating glucose load. As judged from the perfusion pressure vasoconstriction could not account for the inhibitory action. The effect of apomorphine was not reversed by phentolamine infused to block alpha-receptors. Pimozide (1 microM) slightly weakened the inhibitory effect of apomorphine (10 microM) but failed to completely restore a normal secretion. An increase of the pimozide concentration (10 microM) revealed, however, that the agent itself reduced the glucose-induced insulin release. Thus a differentiation of dopamine agonistic and antagonistic effects could not be achieved with the aid of pimozide.

Animals↗

PubMed1978

Influence of intraventricularly applied apomorphine on somato-vegetative reflexes in cats.

To obtain information about the dopaminergic neurotransmission processes taking part in the somatovegetative reflexes the effects of intraventricularly given apomorphine were studied in lightly anaesthetized cats. The level of blood pressure and the reflexogenic hypertension due to central sciatic nerve stimulation were not changed when apomorphine was applied into the lateral and third but was inhibited when given into the fourth ventricle. The nictitating membrane contractions elicited by sciatic nerve stimulation were inhibited by apomorphine when introduced into each part of the ventricular system. Thus the inhibitory dopaminergic synapses located in the structures lining the walls of the brain ventricular system reached by apomorphine appear to be involved in the central control of somato-vegetative reflexes.

Animals↗

PubMed1980

Development of spontaneous motility in chick embryos. Interaction of reserpine and apomorphine.

The effect of apomorphine (1 mg/kg egg weight) on a base of the pre-administration of reserpine (2.5 mg/kg e.w.) 30 min or 2 or 4 hours previously was studied in chick embryos from the 13th to 19th day of incubation. Only the depressant effect of apomorphine was manifested in 13-day embryos. In 15-day embryos summation of the depressant effect of both drugs was recorded for the first time. In 17-day and especially 19-day embryos apomorphine raised the frequency of spontaneous movements high above the level of reserpine-induced depression of motor activity. This activating effect of apomorphine depended upon the supraspinal parts of the CNS, as it disappeared in 17-day embryos after decentralization of the spinal cord (particularly after chronic decapitation). We consider these findings to be further experimental evidence of the participation of catecholaminergic (in particular dopaminergic) central systems in supraspinal control of embryonic motor activity.

Animals↗

PubMed1983

Various dose-dependent influences of apomorphine on the acetylcholine turnover in striatum and mesolimbic areas of rat brain.

The content of acetylcholine and choline and the acetylcholine turnover rates were determined in olfactory tubercle, n. accumbens, striatum and hippocampus after the administration of various doses of apomorphine. Whereas apomorphine failed to change the levels of both amines, the acetylcholine turnover rates were markedly influenced in a dose and time dependent manner. A clear-cut decrease of the latter parameter in all four brain structures was observed after administration of higher doses of apomorphine (1 and 2.5 mg/kg). After a low dose of apomorphine (0.25 mg/kg) the acetylcholine turnover in the striatum was depressed, too. However, the acetylcholine turnover was dramatically increased in olfactory tubercle and n. accumbens. An inhibitory dopaminergic modulation of cholinergic neurons has been postulated to exist in these four brain structures. Some functional differences between the nigrostriatal and the mesolimbic dopamine systems have been discussed.

Acetylcholine↗

PubMed1983

[Features of the effects of apomorphine on rats of different sexes preferring ethyl alcohol].

The influence of apomorphine (1 mg/kg/day subcutaneously) on the behavior and some pharmacokinetic parameters of both male and female rats preferring ethanol to water was studied experimentally. Upon withdrawal of ethanol, apomorphine decreased the time of transmission to water consumption in the rats of both sexes and prevented a decline in the endogenous ethanol levels, the latter effect being especially pronounced in the female rats. Investigations on the "Animex" actograph showed an intensified response to apomorphine in rats preferring ethanol, with female rats displaying a greater change in the response. Under conditions of a renewed access to ethanol, apomorphine increased the time of the restoration of the previous preference for ethanol to water (with a stronger effect seen in females) and lowered the rate of ethanol elimination from the blood (in the female rats exclusively). The effacement of the sex differences in ethanol addicted rats, and a greater damaging impact of ethanol on female rats are emphasized.

Alcoholism↗

PubMed1975

The effect of butaclamol and of other neuroleptic agents on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity.

The effects of the two enantiomers of butaclamol and of several neuroleptics on the apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity was investigated. The (+) but not the (-) enantiomer of butaclamol reverses the apomorphine-elicited enzyme inhibition. (+) Butaclamol is more potent than the other tested neuroleptics. All the tested neuroleptics reverse the apomorphine-elicited enzyme inhibition but their relative potency differs. Using two criteria, namely the concentrations of neuroleptics required to reverse enzyme inhibition maximally or by 25%, the order of decreasing potency is as follows: (+) butaclamol, fluphenazine, haloperidol, pimozide, chlorpromazine. The results suggest that the reversal of apomorphine-elicited inhibition of synaptosomal tyrosine hydroxylase activity is a valid test model for screening antipsychotic drugs.

Animals↗

PubMed1981

[Effect of amizil and galantamin on the behavioral effects of apomorphine in rats].

Stereotypy and locomotor hyperactivity caused by subcutaneous injection of apomorphine (1-5 mg) were quantitated with an "Animex-DSE" motility meter. Intraperitoneal administration of galantamin in a dose of 2.5 mg/kg 10 minutes before apomorphine reversed the latter's effect. However, when injected in a similar way 40 minutes before, it exerted no action on behavioral effects of apomorphine. Intraperitoneal administration of amizyl in a dose of 1 mg/kg completely prevented antagonism of galantamin to apomorphine activity but did not potentiate its effect on the locomotor activity in the animals. The data obtained show that the effect of the cholinergic system on dopaminergic mediation in individual brain structures may be modulating in nature. The experimental data are discussed in the light of the present-day concepts of the function of dopamine receptors in the striatum and mesolimbic systems of the brain.

Animals↗

PubMed1981

An analysis of the effects of apomorphine and haloperidol on the release of [3H]-dopamine and [3H]-noradrenaline from rabbit brain slices.

The effects of apomorphine and haloperidol on the K+-induced release of [3H]-dopamine from striatal slices and [3H]-noradrenaline from cerebellar slices were examined. Apomorphine (0.01-1 microM) reduced the K+-induced release of [3H]-dopamine from striatal slices, leaving the K+-induced release of [3H]-noradrenaline from cerebellar slices unaffected. A higher concentration (10 microM) of apomorphine increased significantly the K+-induced release of [3H]-noradrenaline from cerebellar slices. Haloperidol (0.01-1 nM) increased the K+-induced release of [3H]-dopamine from striatal slices, leaving the K+-induced release of [3H]-noradrenaline unaffected. Haloperidol in higher concentrations (10-100nM) increased significantly the K+-induced release of [3H]-noradrenaline from cerebellar slices. Both compounds inhibited the uptake of [3H]-dopamine into striatal slices and [3H] noradrenaline into cerebellar slices. In low concentrations both compounds showed selectivity for dopaminergic receptor sites, apomorphine stimulating and haloperidol inhibiting pre-synaptic dopamine receptors. Higher concentrations of these compounds showed a non-selective action.

Animals↗

PubMed1981

[Effects of different doses of apomorphine on the glutamate decarboxylase activity of the substantia nigra and the medial basal hypothalamus].

The activity of gamma-aminobutyric acid (GABA) synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) was assayed in the rat substantia nigra (SN) and medial basal hypothalamus (MBH) following systemic injection of different doses of the dopamine receptor agonist apomorphine. In SN, the highest dose of apomorphine (1000 micrograms/kg) causes an increase of the GAD activity whilst an opposite effect is observed with the lowest dose (35 micrograms/kg). Results obtained in SN are in accordance with previous neurochemical and behavioural data suggesting an opposite action of high (500 micrograms/kg) and low doses (100 micrograms/kg) of apomorphine in nigro-striatal system, probably due to the existence of two classes of dopamine receptors, i.e. classical postsynaptic dopamine receptors and presynaptic inhibitory dopamine autoreceptors. In MBH, the evidence for similar effects of low and high doses of apomorphine (the decrease of GAD activity) may suggest that, as already reported, at this level only one class of dopamine receptors is present.

Animals↗

PubMedDate not supplied

Effect of dopamine and apomorphine on bone circulation.

1. The effects of dopamine and apomorphine were studied on the nutrient artery perfusion pressure in dog tibia after constant--flow autoperfusion of the nutrient artery for femoral arterial blood. The carotid arterial pressure was also recorded. 2. Dopamine always induced a rise in nutrient artery perfusion pressure which was reduced or abolished, but never reversed, by alpha-blocking drugs. 3. Apomorphine only elicited a weak and inconstant decrease in the nutrient artery perfusion pressure. Apomorphine vasodilatation was not antagonized by haloperidol, alpha-blocking drugs, sympathetic denervation, propranolol, atropine or mepyramine. Apomorphine induced a non-specific relaxation of the intraosseous vasculature. 4. Thus, this study found with dopamine only a vasoconstrictor effect. These results found no evidence for the existence of dopaminergic receptors in the intraosseous vascular bed.

Animals↗

PubMedDate not supplied

[Effect of apomorphine and haloperidol on the immune reaction].

It has been established that injection of apomorphine leads to the dose-dependent enhancement of the immune response in CBA mice whereas that of haloperidol suppresses the number of rosette-forming cells. After thymectomy apomorphine does not stimulate rosette-formation. This indicates that the thymus participates in the realization of apomorphine action. Preliminary injection of haloperidol prevents the apomorphine-induced enhancement of the immune response. The results suggest that the enhancement is mediated through the activation of dopamine receptors.

Animals↗

PubMed1995

Effect of pimozide on the increase of muscarinic receptors caused by mazindol and apomorphine in the rat cerebral motor cortex.

The effects of pimozide, mazindol and apomorphine on muscarinic receptors in homogenates of rat cerebral motor cortex were measured by binding assays, using 3H-N-methylscopolamine (3H-NMS) alone as ligand (for the measurement of M1- and M2-like receptors) or in the presence of carbachol or pirenzepine for determination of M1- and M2-like receptors, respectively. Female Wistar rats (150 g) were treated daily for one week with pimozide, a dopaminergic antagonist (10 and 20 mg/kg, po, by gavage), or with apomorphine (1 mg/kg, ip). In another set of experiments, animals were treated with pimozide and 30 min later with mazindol (10 mg/kg, po, by gavage) or apomorphine. The drugs were administered daily for one week. Controls received the same volume of saline. 3H-NMS binding was increased from the control value of 418 +/- 17 to 548 +/- 42 fmol/mg protein by administration of mazindol (10 mg/kg) but binding was reduced to 360 +/- 11 fmol/mg protein upon administration of pimozide (20 mg/kg) plus mazindol (10 mg/kg). Similarly 10 mg/kg pimozide reduced the increase in M1-like receptors caused by mazindol from 262 +/- 31 to 220 +/- 20 fmol/mg protein. Although 20 mg/kg pimozide alone produced a decrease in M1- plus M2-like receptors (from 418 +/- 17 to 348 +/- 22 fmol/mg protein), its action was preferentially on M2-like receptors, decreasing them from 148 +/- 10 to 111 +/- 15 fmol/mg protein in the control and treated groups, respectively. At the higher dose, 20 mg/kg pimozide also inhibited the 3H-NMS binding (M1- plus M2-like receptors) in the presence of apomorphine (263 +/- 25 vs 418 +/- 17 fmol/mg protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

[Limited value of the apomorphine test in Parkinson disease].

OBJECTIVE: To determine the predictive value of the subcutaneous apomorphine test for the effect of dopaminergic drugs in the treatment of Parkinson's disease. DESIGN: Retrospective and literature study. SETTING: University Hospital Leiden, the Netherlands. METHODS: All articles regarding apomorphine administration in Parkinson's disease were reviewed. The data were compared with the results of apomorphine tests performed between October 1990 and September 1992 in the Leiden University Hospital. RESULTS: The positive predictive value for good clinical efficacy of dopaminergic medication was 85%, lower than the results from the literature (96%). The negative predictive value was 58% (in the literature 75%), with a sensitivity of 73% and a specificity of 73%. CONCLUSION: These predictive values are poor and practical problems with the test are substantial. Little indication remains for the application of the apomorphine challenge test.

Aged↗

PubMed1994

Apomorphine and diphasic dyskinesia.

We report on three observations of parkinsonian patients with levo-dopa-induced diphasic dyskinesias, who received subcutaneous apomorphine to reduce the duration of abnormal movements. Apomorphine was effective in reducing the duration of diphasic dyskinesias at doses higher than the threshold doses necessary to induce an "on" phase (mean increase: 43%). However, after a few months of treatment, apomorphine was ineffective in stopping abnormal movements, even when doses were increased. In two patients, apomorphine remained effective in the morning, but increased the intensity of the dyskinesias in the afternoon. Acute diurnal variations of the pharmacodynamic striatal response are suggested explanation for these clinical observations.

Aged↗

PubMed1996

Haloperidol and apomorphine differentially affect neuropeptidase activity.

In addition to their well characterized effects at dopamine receptors, neuroleptic drugs have been shown to affect the level and in vitro metabolism of neuropeptides. In the present study, the effect of acute and subchronic administration of the neuroleptic haloperidol and the nonselective, dopamine agonist apomorphine on neuropeptidase activity was determined in regional, rat brain P2 membranes. Subchronic administration of haloperidol decreased the activity of aminopeptidase N in the frontal cortex and caudate-putamen. In contrast, subchronic administration of apomorphine increased aminopeptidase N activity in the frontal cortex and caudate-putamen. Neutral endopeptidase 24.11 also was affected differentially in the caudate-putamen, but both subchronic haloperidol and apomorphine decreased neutral endopeptidase 24.11 activity in the frontal cortex. Metalloendopeptidase 24.15 activity was decreased in the caudate-putamen after acute haloperidol and increased in the frontal cortex after acute apomorphine administration; however, no effect was noted after subchronic administration of either drug. Angiotensin converting enzyme was not affected by any treatment. Therefore, neuroleptic-induced alterations in aminopeptidase N, neutral endopeptidase 24.11 and metalloendopeptidase 24.15 activity may account for previously reported alterations in neuropeptide degradation. In view of the interaction between mesocorticolimbic dopamine neurons and neuropeptides, e.g., substance P, neurotensin and enkephalins, neuroleptic-induced alterations in the activities of neuropeptidases, and thus neuropeptide metabolism can, in turn, play a role in modulating midbrain dopaminergic activity.

Animals↗