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PubMed1986

Influence of naloxone upon apomorphine-induced rotational behavior in rats with electrolytic versus chemolytical lesions of the substantia nigra.

In rats with unilateral electrolytic lesions of the substantia nigra, apomorphine induced ipsilateral rotational behavior that was significantly potentiated by naloxone. Yet, in rats with unilateral chemolytic (6-hydroxydopamine) lesions of the substantia nigra, apomorphine induced dose-dependent contralateral turning that was not influenced by pretreatment with even high doses of naloxone. High performance liquid chromatographic analysis of corpora striata from these rats revealed electrolytically-lesioned animals to have a 60-70% reduction in dopamine content while chemolytically-lesioned animals were virtually completely depleted of dopamine. These results suggest that striatal dopamine may be required for naloxone potentiation of apomorphine-induced effects in the rat rotational behavior paradigm.

Animals↗
PubMed1984

Dissociation of stimulation-bound feeding and apomorphine-induced gnawing by lesions of superior colliculus.

The intense stereotyped gnawing induced by high doses of apomorphine is almost abolished by large bilateral lesions of the superior colliculus. It has been argued that the feeding produced by electrical stimulation of the lateral hypothalamic area is closely related to dopamine-mediated oral stereotypies; if so, it might be expected that lesions of the superior colliculus would also disrupt stimulation-bound feeding. Feeding was obtained from 14 hypothalamic electrodes in 8 hooded Lister rats. Subsequent electrolytic lesions of the superior colliculus had no overall effect on this behaviour from 13 of the 14 electrodes, even though the lesions reduced the gnawing induced by 8-20 mg/kg apomorphine to less than 10% of its preoperative intensity. It is concluded that stimulation-bound feeding and apomorphine-induced gnawing are not dependent on identical neural circuitry, and therefore stimulation-bound feeding is probably not mediated by the nigrotectal pathway.

Animals↗
PubMed1984

Administration of small doses of apomorphine attenuates feeding in non-deprived pigeons.

The dopamine agonist apomorphine was administered peripherally at small doses of 25, 50 or 100 micrograms to non-deprived pigeons, either in the morning or in the afternoon. The food and water consumption of the birds was then measured at 4 times (30, 60, 90 and 120 min) after the injection. In the control condition (injection of saline), the pigeons ate less in the morning than in the afternoon, whereas a reverse situation was observed for drinking. Administration of apomorphine attenuated the food consumption in a dose-related fashion, at both times of the day, and for no longer than 90 min post-injection; the reduction of feeding was relatively larger when the drug was given in the morning than in the afternoon, and it was not accompanied by consistent changes of the water consumption. These results show that in pigeons, the feeding-like responses to apomorphine treatment (pecking, swallowing, mandibulating) which have been described previously are not associated with an actual enhancement of the food intake. Possible mechanisms and loci of action of dopamine agonists on these 2 types of behaviors are discussed.

Animals↗
PubMed1986

Dose-related response of male rats to apomorphine: snout contact in the open-field.

Apomorphine (0.01 to 5 mg/kg, SC) was administered to male rats observed singly in the open-field. The behavior of each rat was coded using a microprocessor during 3 preinjection and 9 postinjection trials of 6 min duration over a 2 hr session. The behavior categories included grooming, yawning, turning, nodding and gnawing, as well as snout contact and nonsnout contact variants of locomoting, rearing and sitting. Dose-dependent increases in the time spent in snout contact with the field surface were noted throughout the complete dose range. Both the peak and duration of the snout contact epoch increased with the dose of apomorphine. The integrated time spent in all types of snout contact proved to be the best behavioral measure for discriminating between doses of apomorphine even though the topography of snout contact response changed as a function of the dose.

Animals↗
PubMed1989

Neuroleptic-induced emotional defecation: effects of pimozide and apomorphine.

Neuroleptics, such as haloperidol, have been found to produce dysphoria, anxiety and akathisia in humans. In animals, these effects have rarely been reported since the decreased movement produced by these drugs can confound the study of many behavioral indices of emotionality. In fact, most investigators have found a decrease in emotional defecation in rats given neuroleptics in novel environments, supporting their action as a major tranquilizer. We have found, however, that in rats a profound increase in emotional defecation can result from haloperidol administration in well habituated environments, such as the homecage. In male rats, defecation was measured for a one hour test period following various doses of the neuroleptic, pimozide, and the dopamine receptor agonist, apomorphine. Apomorphine and pimozide (a dopamine receptor antagonist) were both found to increase levels of fecal boli excretions. In addition, when apomorphine was combined with haloperidol, defecation levels were also increased suggesting that this phenomenon is not directly mediated by dopamine receptors. It is suggested that this drug-induced defecation is a consequence of the agent's interaction with the affective state of the animal, creating a dysphoric or anxious state in the animal.

Animals↗
PubMed1979

"Classical" and "atypical" antipsychotic drugs: differential antagonism of amphetamine- and apomorphine-induced alterations of spontaneous neuronal activity in the neostriatum and nucleus accumbens.

The ability of clozapine and haloperidol to antagonize the depression of firing rate produced by d-amphetamine and apomorphine in the neostriatum and nucleus accumbens was tested in immobilized, locally anesthetized rats. In the neostriatum, an intraperitoneal injection of 2.5 mg/kg d-amphetamine or 1.0 mg/kg apomorphine produced a prolonged inhibition of neuronal activity that was reversed by a subjsequent injection of either 20 mg/kg clozapine or 2.0 mg/kg haloperidol. An analysis of the onset and magnitude of the blockade revealed that clozapine was more effective than haloperidol in reversing the amphetamine response but that both antipsychotic drugs produced a comparable blockade of the apomorphine-induced depression. Similar results were obtained in the nucleus accumbens. The data indicate that although clozapine acts equieffectively in the neostriatum and nucleus accumbens, this atypical antipsychotic drug, aside from blocking postsynaptic dopamine receptors, may exert at least some of its effects by preventing dopamine release.

Amphetamine↗
PubMed1980

Effects of thioridazine on apomorphine-elicited stereotypic behavior and motor activity.

Bilaterally injected thioridazine (10 micrograms) into the striata of rats augmented the stereotypic behavior elicited by apomorphine. The enhancing effect was attenuated by pretreatment with alpha-methyl-p-tyrosine. At 48 hr postinjection of thioridazine (1.0 mg/kg, IP), motor suppression from a low dose of apomorphine (0.2 mg/kg, IP) was enhanced; however, motor response to a high dose of apomorphine (1 mg/kg, SC) was not affected. Possible mechanisms of action of thioridazine are discussed.

Animals↗
PubMed1982

Influence of estrogen and progesterone on behavioral effects of apomorphine and amphetamine.

A study was made of the influence of apomorphine. D- and L-amphetamine on the effects of different hormonal treatments used to induce copulatory behavior in female rats. Female copulatory behavior, (lordosis response), which has been shown to be inhibited by increased DA and 5-HT neuronal activity, was depressed by apomorphine, D- and L-amphetamine in ovariectomized rats treated with estrogen + progesterone. When lordosis behavior was activated by estrogen alone the inhibitory action of the drugs, especially that of apomorphine was considerably less pronounced. However, the effect of D-amphetamine on stereotype activity was not greater after treatment with estrogen + progesterone than after administration of estrogen alone. Estrogen had a slight stimulatory effect on stereotype activity in non-drug-treated rats, while progesterone had an inhibitory effect. Possible mechanisms underlying the observed interactive effect of progesterone and monoamines on lordosis behavior, such as a progesterone-induced alteration of monoaminergic transmission, are discussed.

Amphetamine↗
PubMed1982

Effects of apomorphine on appetitive conditioning in 6-hydroxydopamine treated rat pups.

Rat pups were treated on postnatal day 5 either with the combination of desmethylimipramine (DMI) and 6-hydroxydopamine (6-OHDA) to produce depletion of brain dopamine, or with control injections of saline. Two days later they were presented a novel anise odor paired with intraoral baby formula, and on the next day were tested for preference for the novel odor. Before conditioning and testing, animals were treated with either apomorphine (0.05 mg/kg) or isotonic saline. Performance of the conditioned appetitive response was impaired in dopamine depleted animals. In DMI/6-OHDA treated pups, apomorphine administration prior to conditioning produced an improvement in performance, but drug treatment prior to testing had no effect. In normal pups, apomorphine administration either before conditioning or testing produced impaired performance at testing.

Animals↗
PubMed1982

A quantitative analysis of stereotyped gnawing induced by apomorphine.

An apparatus was designed and constructed to enable a quantitative analysis of the stereotyped gnawing produced by the dopamine agonist apomorphine. Using this apparatus it was discovered that increasing the subcutaneous dose of apomorphine increased (1) the number of animals that gnawed, and (2) the duration of gnawing in those animals that gnawed at all doses. Other aspects of apomorphine-induced gnawing, in particular the latency to respond and the frequency and duration of individual gnaws, were relatively unaffected. Likely properties of the system responsible for the organization of sterotyped gnawing are discussed.

Animals↗
PubMed1982

Apomorphine-induced facilitation of intracranial self-stimulation following dopamine denervation of the nucleus accumbens.

Two groups of rats were trained to lever press for intracranial self-stimulation (ICSS) from electrodes aimed at the posterior lateral hypothalamus or at the region of the locus coeruleus. Following stabilization of baseline responding using descending rate/intensity functions, bilateral 6-hydroxydopamine (6-OHDA) lesions to the nucleus accumbens (N.Acc.) were performed. Subsequent injections of apomorphine (SC) resulted in significant increases in self-stimulation in both lesion groups and significant decreases in self-stimulation in both groups of sham operated animals. These results indicate that the destruction of the dopaminergic terminals in the nucleus accumbens results in a "supersensitive" enhancement of the ICSS stimulating properties of apomorphine regardless of the electrode placement. Both lesion groups also showed a pronounced increase in locomotor activity in photocell cages following treatment with the same dose of apomorphine. These results complement previous work showing that dopamine destruction affects ICSS regardless of electrode placement and support the hypothesis that the midbrain dopamine systems have a general response enabling role in reinforced behavior.

Animals↗
PubMed1983

Potentiation of apomorphine-induced stereotypies by naloxone and L-prolyl-L-leucyl-glycinamide.

We compared the influences of pretreatment with the narcotic antagonist drug naloxone and the neuropeptide L-prolyl-L-leucyl-glycinamide (PLG) upon apomorphine-induced stereotypic climbing activity in mice and apomorphine-induced contralateral rotational behavior in rats with unilateral 6-hydroxydopamine lesions of the substantia nigra. Naloxone produced dose-related potentiation in the mouse climbing model, while PLG was without effect. On the other hand, PLG produced dose-related potentiation in the rat rotational paradigm, while naloxone was without appreciable influence. These findings show an asymmetrical potentiation of apomorphine by naloxone and PLG in these two standard experimental models of striatal dopaminergic activity.

Animals↗
PubMed1983

Spontaneous and apomorphine-induced locomotor changes parallel dopamine receptor differences in two rat strains.

Two inbred strains of rats (F344 and Buffalo) were tested for differences in spontaneous and apomorphine-induced inhibition of locomotor activity. F344 rats showed greater percentage decreases in locomotion after apomorphine (0.25, 1.0 and 2.5 mg/kg) compared to the Buffalo strain. F344 rats also showed higher levels and slower habituation of spontaneous locomotor activity. F344 rats had previously been shown to have significantly higher densities of D2-dopamine receptors in the striatum and olfactory tubercle and also more apomorphine-induced stereotypy when compared to Buffalo rats. These results confirm and extend previous studies suggesting that genetic differences in brain D2-dopamine receptors can predict behavioral differences in locomotor activity.

Animals↗
PubMed1983

Hypophysectomy prevents yawning and penile erection but not hypomotility induced by apomorphine.

A small dose of apomorphine (25 or 50 micrograms/kg, SC) induced repeated episodes of yawning, penile erection, genital grooming and a decrease in locomotor activity in rats. Hypophysectomy almost completely abolished yawning, penile erection and genital abolished yawning, penile erection and genital grooming but failed to modify the hypomotility induced by apomorphine. These results suggest that pituitary hormones are directly or indirectly involved in the apomorphine-induced yawning, penile erection and genital grooming but not in the sedative response to this drug.

Adrenocorticotropic Hormone↗
PubMed1983

A caerulein-sensitive potentiation of the behavioral effects of apomorphine by dibutyryl-cAMP.

The dopaminergic behavioral effects of apomorphine in rats were evaluated using a rating scale. Caerulein, a decapeptide physiologically similar to cholecystokinin, enhanced at lower doses and inhibited at higher doses the behaviors induced by apomorphine. Dibutyryl-cAMP, but not dibutyryl-cGMP, potentiated apomorphine behaviors. This potentiation was inhibited by a high dose of caerulein. These data provide evidence for an opposing effect of cAMP and caerulein or cholecystokinin in modulating dopaminergic systems.

Animals↗
PubMed1983

Stereotyped behavior affected by peripheral and intracerebroventricular apomorphine administration in pigeons.

In pigeons, peripheral injection of apomorphine HCl (1.5 mg) produced a rapid pecking response while intracerebroventricular administration of the drug (60 micrograms) was ineffective in this respect. Both peripheral and to a larger extent central treatment with apomorphine stimulated another activity, that is headshaking. The frequency of other behavioral patterns was either decreased (preening) or unaffected (yawning, stretching) following both treatments. Together with previous studies, these data suggest that (a) apomorphine stimulates pecking in pigeons by activating dopaminergic mechanisms lying in brain areas situated away from the ventricles; (b) dopaminergic mechanisms situated in periventricular regions may take part in the control of some patterns, e.g. headshaking, and (c) other activities do not appear to depend directly on these mechanisms.

Animals↗
PubMed1985

Effect of chronic apomorphine on the development of denervation supersensitivity.

We hypothesised that it would be possible to prevent the development of post-synaptic dopamine receptor supersensitivity to 6-hydroxydopamine lesions of the nigro-striatal tract in rats if they were constantly infused with the dopamine agonist apomorphine. Using osmotic minipumps to infuse apomorphine for 15 days in unilaterally lesioned rats, it was possible to delay the development of supersensitivity of the lesioned side for 9 days but not to prevent its eventual appearance. At the same time, evidence for the development of subsensitivity of presynaptic dopamine receptors of the intact side following chronic infusion of apomorphine was inferred from the production of rotations directed towards the lesioned side.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Apomorphine increases ethanol discrimination.

Rats were trained to discriminate between the stimulus properties of 600 mg/kg ethanol and saline in a two-lever, food-motivated operant task. Once trained, rats showed a dose-related decrease in discriminative performance with lower ethanol doses and analysis of the dose-response curve indicated an ED50 of 372 mg/kg. Pretreatment with 0.16 mg/kg apomorphine produced increased discriminative performance at each ethanol dose and the combination generated a dose-response curve parallel to ethanol administered alone with an ED50 of 232 mg/kg. This significant shift to the left of the ethanol dose-response curve after apomorphine administration is discussed in relation to dopaminergic neuronal systems and the clinical use of apomorphine alcoholics.

Animals↗