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PubMed1984

Neuropeptides related to neurohypophyseal hormones interfere with apomorphine-induced behavioral changes.

The interaction between peptides related to neurohypophyseal hormones and brain dopaminergic systems was studied by investigating in rats the effect of these peptides on behavioral changes induced by graded doses of the specific dopamine agonist apomorphine. Low doses of this drug induce hypoactivity of the animals, while higher doses result in hyperactivity and stereotyped sniffing. Desglycinamide9[Arg8]vasopressin (DG-AVP), prolyl-leucyl-glycinamide (PLG) and oxytocin did not interfere with the behavioral responses induced by the higher doses of apomorphine. Peptide treatment made the rats more sensitive to apomorphine with respect to the drug induced hypoactivity. PLG and especially DG-AVP were more effective than oxytocin. It is concluded that these peptides may have a selective action on distinct dopaminergic receptor systems in the brain, that are presumably located presynaptically in the nucleus accumbens area.

Animals↗

PubMed1984

Neuroendocrine responses to apomorphine in depressed patients and healthy control subjects.

Increasing evidence implicates altered dopamine function in major affective illness. In the present study, growth hormone responses to the dopamine agonist apomorphine were not different for 14 male depressed patients and 16 healthy male volunteers. Baseline and post-apomorphine prolactin levels were lower for the depressed patients than the control subjects, but the percent decrease following apomorphine was not different for the two groups. Neuroendocrine responses were not significantly altered during chronic treatment with the dopamine agonist piribedil. These neuroendocrine results suggest that decreased baseline prolactin levels in depressed patients do not reflect altered postsynaptic receptor sensitivity in the tuberoinfundibular dopamine system.

Adult↗

PubMed1986

Relationship of psychotic symptom clusters in schizophrenia to neuroleptic treatment and growth hormone response to apomorphine.

The authors propose an alternative model for relating clinically rated psychotic symptoms to biological measures in schizophrenic patients. They suggest that clinical presentation in schizophrenic patients comprises at least four distinct psychotic symptom clusters and that at most one or two of the symptom clusters are closely associated with central dopamine (DA) activity as measured by growth hormone (GH) response to apomorphine. Factor and cluster analytic techniques both identified the same four psychotic symptom clusters, three of which were similar to the major subtypes of schizophrenia: paranoid delusions (paranoid type), thought disorder (disorganized type), and catatonia (catatonic type). The fourth psychotic symptom cluster was auditory hallucinations, a prominent clinical feature of schizophrenia. The authors compared clinical symptom cluster scores to apomorphine-induced GH response by creating a new data set containing the output of the factor analysis of each patient's symptoms and GH response, and performing regression modeling of the patient's symptom cluster scores on GH response. Patients with elevated thought disorder cluster scores also had elevated GH responses to apomorphine, suggesting an association between thought disorder and central DA receptor supersensitivity. A fixed-dose neuroleptic trial showed that thought disorder and auditory hallucinations respond rapidly to treatment with a DA receptor blocker (haloperidol), while no significant effect on other symptom cluster scores occurred during the initial 2 weeks of treatment. These data suggest that two of the identified symptom clusters, thought disorder and auditory hallucinations, may be preferentially associated with central DA hyperactivity.

Adolescent↗

PubMed1988

Neuropeptide-dopamine interactions. II. Cyclo (His-Pro) augmentation of amphetamine- but not apomorphine-induced stereotypic behavior.

Histidyl-proline diketopiperazine (cyclo [His-Pro]) not only exists in the basal ganglia of rodents, monkeys, and humans, but also exhibits a variety of biologic activities, some of which appear to be mediated via dopaminergic mechanisms. We investigated the potential modulation by cyclo (His-Pro) of amphetamine- and apomorphine-induced stereotypic behavior, a behavior that is associated with the activation of postsynaptic dopamine receptor. Administration of amphetamine to rats resulted in a dose-dependent increase in stereotypic behavior that was further augmented if animals were pretreated with cyclo (His-Pro). Although apomorphine also led to a dose-related progression in the stereotypic behavior, the apomorphine effects were not modified by cyclo (His-Pro) pretreatment. We conclude that cyclo (His-Pro) either acts indirectly at the presynaptic dopamine site or modulates other neurotransmitters to potentiate actions of amphetamine.

Amphetamine↗

PubMed1990

Effects of intrastriatal apomorphine on changes in switching behaviour induced by the glutamate agonist AMPA injected into the cat caudate nucleus.

Bilateral intracaudate application of the glutamate agonist DL-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA), viz. an agonist of quisqualate receptors, is known to produce the following effects in cats that had to climb on a small wooden bar and, subsequently, to switch to distinct patterns: it produces increases in switching from one pattern to another pattern (1) and it induces limb deficits, i.e. unilateral deficient placing of the fore- and/or hindlimb. In the present study, the effect of stimulating striatal dopamine receptors on behavioural changes induced by intracaudate injections of AMPA was investigated. Therefore, the dopamine agonist apomorphine was injected into the caudate nucleus 5 min before the striatal injection of 1.0 micrograms AMPA. AMPA-induced increases in switching behaviour were prevented by 0.6 micrograms, but not 0.3 micrograms, apomorphine. In contrast, AMPA-induced limb deficits were not prevented by pretreatment of apomorphine. In view of the notion that the dopaminergic caudate nucleus, its output station the substantia nigra, pars reticulata and the nigral output station the deeper layers of the colliculus superior are essential for switching behaviour, but not for the display of disturbances like AMPA-induced limb deficits, the present data strongly suggest that only AMPA-induced changes in switching, but not AMPA-induced limb deficits, are mediated by the caudato-nigro-collicular circuitry. The glutamate receptor-selectivity of the modulatory action of dopamine is discussed.

Afferent Pathways↗

PubMed1987

Haloperidol prevents the methamphetamine-induced apomorphine subsensitivity of dopamine metabolism in rat striatum.

Our previous experiment showed that the sensitivity of striatal dopaminergic metabolism to apomorphine was lowered after pretreating rats with methamphetamine. This study further demonstrated that haloperidol administered with methamphetamine prevented the effect of the methamphetamine pretreatment. Since gamma-butyrolactone was administered in combination with apomorphine so as to remove complications which might arise from the modification of impulse flow through the striatonigral feedback loop, it is possible that the observed effect of apomorphine upon striatal dopaminergic metabolism and its antagonism with haloperidol may be mediated by autoreceptors of dopaminergic axon terminals in rat striatum.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1995

Median nerve somatosensory evoked potentials. Apomorphine-induced transient potentiation of frontal components in Parkinson's disease and in parkinsonism.

Somatosensory evoked potentials (SEPs) to median nerve stimulation have been recorded from parietal and frontal districts in 43 parkinsonians, 17 patients with parkinsonism and 35 healthy controls matched for age and sex. Latency/amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and after (10, 20, 30 and 60 min) subcutaneous administration of apomorphine chloride were evaluated in all the 60 patients and in 3 controls. The frontal waves N30 and P40 were either absent or significantly smaller than normal in 31 patients with Parkinson's disease (PD) (72.1%) and in 9 with parkinsonism in baseline records (56.3%). Following apomorphine, the parietal deflections did not significantly vary in amplitude. On the contrary, the frontal complex showed a significant amplitude increase in 27 PD and 8 parkinsonisms (respectively 62.8 and 47.1%); 79.1% of PD and 35.3% of parkinsonisms were improved clinically. Amplitude increase was evident at 10 min after apomorphine, in parallel with clinical improvement, and vanished nearly in coincidence with the end of the clinical effect.

Adult↗

PubMed1983

Potentiation of apomorphine-induced gnawing in mice.

1. The association of antagonism of apomorphine-induced climbing with potentiation of apomorphine-induced gnawing in mice has been suggested as a means to detect "atypical" neuroleptics. 2. Clozapine, many compounds with central anticholinergic activity and propranolol have been demonstrated to possess this profile of activities. 3. Pharmacological manipulations with cholinomimetics suggest a cholinergic modulation of the gnawing behavior induced by apomorphine. 4. The observations with propranolol cannot be explained either by a cholinergic link nor by beta-adrenergic antagonism.

Animals↗

PubMed1988

Apomorphine-induced vomiting in rainbow trout (Salmo gairdneri).

1. The LD50 for a 7-day period following intraperitoneal injection of apomorphine-HCl was calculated to be 158 mg/kg in rainbow trout. 2. Intraperitoneal injection of apomorphine at doses of 60 mg/kg or greater caused vomiting of plastic balls which had been placed in the stomachs of rainbow trout. 3. Apomorphine-induced effects included vomiting, vomiting behavior, toxicity, increased respiration, impaired motor control and equilibrium, and increased aggression. 4. The vomiting control mechanism of trout may be similar to that described in mammals.

Aggression↗

PubMed1980

Differential effects of ageing on distinct features of apomorphine stereotypy in the adult rat.

Locomotor features of stereotypy induced by 0.15 mg/kg of subcutaneous apomorphine increased over the age ranges of 2.5-8 and 8-10 months in the adult rat. Perioral features of stereotypy induced by 1 mg/kg of apomorphine, and spontaneous activity did not show age-dependent changes. Heterogeneous features of apomorphine stereotypy may have distinct physiological substrates that are differentially sensitive to parameters of maturation and ageing.

Aging↗

PubMed1986

Responsiveness to 'autoreceptor' doses of apomorphine inversely correlated with the firing rate of dopaminergic A9 neurons: action of baclofen.

Supersensitivity of dopamine (DA) autoreceptors develops soon after acute treatments with baclofen or gamma-butyrolactone, two drugs which suppress DA neuronal firing. We have hypothesized that this effect might reflect a condition associated with the low firing rate of DA cells induced by such treatments rather than a long-term adaptive modification of DA receptor sensitivity. In this study we show that the degree of the intravenous apomorphine-induced inhibition of A9-DA neurons is inversely correlated to the basal firing rate of these neurons. When administered after baclofen, apomorphine further reduced DA cell activities in a manner proportional to the predrug firing rate, as in control rats. Since the minute doses of apomorphine which were used are thought to selectively activate DA autoreceptors, our finding may indicate that DA autoreceptor stimulation is more effective when the activity of the DA neurons is low, or it is decreased by drugs such as baclofen.

Animals↗

PubMed1989

Apomorphine increases plasma oxytocin concentration in male rats.

The effect of systemic administration of the dopamine agonist apomorphine on plasma oxytocin concentration was studied in male rats by a specific radioimmunoassay. Apomorphine given subcutaneously in doses ranging from 80 to 480 micrograms/kg increased oxytocin levels in a dose-dependent manner. The minimal effective dose was found to be 80 micrograms/kg, which induced a 66% increase above basal values, while the maximal effect (210%) was seen with a dose of 240 micrograms/kg. The apomorphine effect was prevented by pretreatment with the DA D2-receptor blockers haloperidol (0.2 mg/kg i.p.) or (-) sulpiride (10 mg/kg i.p.) and, but only partially, with the DA D1-receptor blocker SCH 23390 (0.2 mg/kg s.c.). The present results suggest that hypothalamic dopamine has a facilitatory role on the release of oxytocin in male rats.

Animals↗

PubMed1989

Apomorphine-induced inhibition of substantia nigra dopamine neurons: effects of unilateral injection through the internal carotid artery.

Possible indirect components in the inhibition of firing of A9 dopamine neurons induced by systemic apomorphine were studied using unilateral drug administration through the internal carotid artery, known to irrigate only the ipsilateral mid- and forebrain. When compared to intravenous injection, unilateral intracarotid administration inhibited ipsilateral neurons with a marked decrease of both the latency (less than 1 s) and the dose required for complete inhibition, whereas contralateral neurons were not affected. This suggests a first-pass central effect of apomorphine, presumably associated with brain extraction. Thus, peripheral and hindbrain targets do not seem to contribute to the inhibitory effect of low doses of systemic apomorphine. An intranigral possible mode of action is discussed in view of the particular arrangement of dopaminergic dendrites within the zona reticulata.

Action Potentials↗

PubMed1987

The oxidation of apomorphine and other catechol compounds by horseradish peroxidase: relevance to the measurement of dihydropteridine reductase activity.

It has been reported by Shen et al. (Shen, R.-S., Smith, R.V., Davis, P.J. and Abell, C.W. (1984) J. Biol. Chem. 259, 8894-9000) that apomorphine and dopamine are potent, non-competitive inhibitors of quinonoid dihydropteridine reductase. In this paper we show that apomorphine, dopamine and other catechol-containing compounds are oxidized rapidly to quinones by the horseradish peroxidase-H2O2 system which is used to generate the quinonoid dihydropterin substrate. These quinones react non-enzymatically with reduced pyridine nucleotides, depleting the other substrate of dihydropteridine reductase. When true initial rates of dihydropteridine reductase-dependent reduction of quinonoid dihydropterins are measured, neither apomorphine nor any other catechol-containing compound that has been tested has been found to inhibit dihydropteridine reductase.

Animals↗

PubMed1983

Effects of apomorphine administration on locomotor activity of control and experimental rats withdrawn from long-term haloperidol treatment.

Rats were administered increasing doses of haloperidol or control solution for 25 days, 72 hr after drug withdrawal they were observed for locomotor activity in an open field with and without apomorphine treatment. Locomotion frequency was higher in haloperidol withdrawn rats. In both groups locomotion frequency decreased 15 min after apomorphine administration, in a dose-dependent way. Apomorphine induced, also, different motor effects not necessarily similar in control and experimental rats. Supersensitivity of dopaminergic receptors induced by the long-term neuroleptic administration was considered to be involved with the differences observed.

Animals↗

PubMed1996

Apomorphine and dopamine D(1) receptor agonists increase the firing rates of subthalamic nucleus neurons.

The present study investigated the regulation of spontaneous neuronal activity in the subthalamic nucleus by dopamine receptors using in vivo extracellular single unit recording techniques. Subthalamic nucleus neuronal firing rates were doubled by systemic administration of the nonselective dopamine receptor agonist apomorphine. The response to apomorphine was attenuated in animals anesthetized with chloral hydrate or ketamine. The dopamine D(2)/D(3) receptor agonist quinpirole did not alter subthalamic nucleus neuronal firing rates. Firing rates were increased by the D(1) receptor agonists SKF 38393 and SKF 82958 two- to three-fold; these increases were reversed by the D(1) receptor antagonist, SCH 23390. Autoradiographic studies using [(125)I]SCH 23982 indicated that D(1) family receptors were located along the ventral edge of the subthalamic nucleus and the dorsal aspect of the cerebral peduncle. Local administration of SKF 82958 into the subthalamic nucleus doubled neuronal firing rates; these increases were reversed by systemic administration of SCH 23390. Infusion of SCH 23390 into the subthalamic nucleus prevented systemic SKF 38393 from increasing the firing rates of subthalamic nucleus neurons. These results indicate that apomorphine and D(1) receptor agonists exert an excitatory influence on subthalamic nucleus neuronal activity. In addition, the excitation induced by D(1) receptor agonists appears to be mediated, at least in part, by D(1) receptors located in the vicinity of the subthalamic nucleus. The data suggest that basal ganglia output under conditions of increased dopamine receptor stimulation is influenced by the activation of excitatory subthalamic efferent pathways, as opposed to suppression of these pathways as predicted by current models of basal ganglia function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1992

Apomorphine stimulation of vasopressin- and oxytocin-neurophysins. Evidence for increased oxytocinergic and decreased vasopressinergic function in schizophrenics.

Apomorphine challenge tests (0.5 mg SC) were performed in 14 normal male volunteers and in 9 male schizophrenic inpatients, drug-free for at least 2 wk. In the normal volunteers, apomorphine induced an increase of serum growth hormone (GH) (maximum at 40 min), of vasopressin-neurophysin (hNpI) (maximum at 20 min), and oxytocin-neurophysin (hNpII) (maximum at 20 min). The release of neurophysins was independent of digestive side effects. In the schizophrenics, the GH level and release pattern were similar to those in the controls. The basal level of hNpI was reduced (t0: 0.42 +/- 0.1 ng/ml in the schizophrenics and 0.66 +/- 0.05 ng/ml in the controls, p < 0.02). In contrast, the basal level of hNpII was increased (3.34 +/- 0.04 ng/ml in the schizophrenics to 0.92 +/- 0.21 ng/ml in the controls, p = 0.001). The response to apomorphine was blunted, with no significant release of hNpI or of hNpII. Although the hNpII data are consistent with an increased dopaminergic tone, the psychopathological meaning of the increased basal oxytocinergic and decreased vasopressinergic functions remains to be defined.

Adult↗

PubMed1987

Small apomorphine-induced increase in the concentration of cytosol estrogen receptors in female rat hypothalamus and pituitary.

A series of experiments was performed to investigate the previously-reported modulation of estradiol binding in female rat brain and pituitary gland by drugs that influence the dopaminergic system. Injection of the dopamine agonist, apomorphine, at minimum doses of 1-2 mg/kg body weight caused slight increases (in most cases, less than 10%) in the concentration of cytosol estrogen receptors in the mediobasal hypothalamus and anterior pituitary gland without influencing the concentration in the preoptic area. However, after subsequent injection of a saturating dose of estradiol, the level of nuclear estrogen receptors accumulating did not differ significantly between apomorphine-treated animals and vehicle-injected controls. These results extend, in part, previous reports that have shown an apomorphine-induced increase in the concentration of [3H]estradiol in brain and pituitary cell nuclei after an injection of [3H]estradiol. However, we failed to observe differences in the concentration of cytosol estrogen receptors as large as would be expected by previous work, and we failed to observe differences in the concentration of nuclear estrogen receptors after estradiol injection.

Animals↗