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At least 937 records · Page 52Linked to original sources
PubMed1984

Behavioural responsiveness to muscimol and apomorphine 2 months after prolonged treatment with estradiol in rats.

Two months after prolonged administration of estradiol (ES) in female rats the behavioural responsiveness to muscimol, a GABA receptor stimulating agent, and to apomorphine, a dopamine receptor agonist, was significantly altered. In particular, the decrease in locomotor activity induced by a challenge dose of muscimol (0.5-1 mg/kg) was significantly attenuated in ES-pretreated animals. Conversely, the intensity of stereotyped behaviour elicited by a challenge dose of apomorphine (1 mg/kg) was significantly increased in ES-pretreated rats. The behavioural alterations in the response to muscimol and apomorphine presumably result from the production of central GABA receptor subsensitivity and dopamine receptor supersensitivity respectively, induced by the prolonged ES administration.

Animals↗
PubMed1984

Differences in the stereotypy response but not the hypomotility response to apomorphine in the Roman High and Low avoiding strains of rats.

Two experiments were carried out to investigate differences in the behavioural responses to "high" and "low" doses of apomorphine in two strains of rats selectively bred for high and low avoidance on a two-way active avoidance task: the Roman High and Low Avoiders. Significant strain differences were found in the stereotypy resulting from a high dose of apomorphine (2 mg/kg s.c.). In a second experiment no strain differences were, however, apparent for the hypomotility produced by low doses of the drug (0.05 mg/kg s.c.). Pretreatment with a low dose of apomorphine had no effect on the stereotypy response when the animals were subsequently retested with the high dose. These results may indicate differential sensitivities of dopamine receptors in these strains.

Analysis of Variance↗
PubMed1985

Repeated treatment with imipramine potentiates the locomotor effect of apomorphine administered into the hippocampus in rats.

The effect of apomorphine, injected into the dorsal hippocampus, on the locomotor activity of imipramine-treated rats was studied. The rats were chronically implanted with cannulae 1 week before imipramine treatment. Imipramine was given in a dose of 10 mg/kg per os, acutely, or twice a day for 14 days. Intrahippocampal injection of apomorphine induced a dose-dependent increase in locomotor activity. This effect was antagonized by pretreatment with pimozide (2 mg/kg). Repeated, but not single, administrations of imipramine significantly enhanced the apomorphine-induced locomotor hyperactivity in rats. This effect was observed at 2, 48 and 96 h after the last dose of imipramine. The results obtained indicate that repeated administration of imipramine increases the responsiveness of the hippocampal dopaminergic system.

Animals↗
PubMed1984

The effect of amitriptyline treatment on the growth hormone response to apomorphine.

The growth hormone response to subcutaneous administration of the dopamine agonist apomorphine (0.005 mg/kg) was assessed in six normal male subjects before and at the end of a course of amitriptyline. Amitriptyline treatment significantly reduced the growth hormone response to apomorphine, confirming the findings of an earlier study in depressed patients. The way in which amitriptyline attenuates the effect of apomorphine is not clear. Direct blockade of dopamine receptors in the hypothalamus is a possibility, but long-term amitriptyline treatment could result in adaptive changes in the monoamine pathways which control GH release.

Adult↗
PubMed1979

Dimethylaminoethanol (deanol): effect on apomorphine-induced stereotypy and an animal model of tardive dyskinesia.

Dimethylaminoethanol (DMAE) was administered acutely to rats subsequently injected with spomorphine. A dose of 80 mg of DMAE had no effect on the severity of apomorphine-induced stereotypy. However, 160 mg of DMAE significantly diminished the severity of apomorphine-induced stereotypy. This dose of DMAE did not significantly alter spontaneous locomotor activity. DMAE did not reduced apomorphine-induced stereotypy in animals previously exposed to haloperidol and presumed to have postsynaptic dopamine receptor supersensitivity. These results with DMAE are contrasted with the effects of choline chloride, and suggest that choline chloride may be more effective than DMAE at augmenting striatal cholinergic activity.

Animals↗
PubMed1985

Yawning elicited by systemic and intrastriatal injection of piribedil and apomorphine in the rat.

The behavioural effects of systemic and intrastriatal injections of the dopamine agonists piribedil and apomorphine in male rats were examined. Bilateral application of piribedil (50 and 100 micrograms) or apomorphine (5, 10 and 20 micrograms) to the striatum produced yawning and chewing mouth movements accompanied by intermittent stretching and sexual arousal. Low doses of piribedil (1.25 and 2.5 mg/kg) and apomorphine (0.1 and 0.2 mg/kg) injected SC produced an identical yawning syndrome. Previous work has suggested that yawning elicited by systemic dopamine agonist treatment is a consequence of dopamine autoreceptor stimulation. Similarly, the most likely explanation of the present data is that yawning elicited by systemic and central dopamine agonist treatment was due to activation of dopamine autoreceptors. Systemic injection of haloperidol and scopolamine abolished yawning induced by intrastriatal piribedil and these data provide tentative support for the proposal that a dopamine-acetylcholine link may be involved in the expression of yawning.

Animals↗
PubMed1980

Effects of apomorphine on elicited and operant pecking in pigeons.

The effects of apomorphine (0.001--32.0 mg/kg) on elicited and operant pecking were studied in pigeons. Elicited pecking was measured in a 1-h observation test. Apomorphine caused dose-related increases in the pecking elicited by the drug in all the subjects, with maximal responding at 3.2 mg/kg. In contrast, operant responding on a multiple, 5 min fixed interval, 30 response fixed-ratio schedule revealed individual differences in sensitivity to the drug. A dose of 0.32 mg/kg eliminated key pecking in fixed-interval and fixed-ratio components in 4 (group 1) of the 15 subjects while 3.2 mg/kg eliminated responding in 9 other subjects (group 2), and 2 of the subjects (group 3) required 32.0 mg/kg to eliminate responding. The 13 birds in groups 1 and 2 showed decreases in operant responding with concomitant increases in elicited pecking. For the 2 remaining birds, increases in operant behavior were highly correlated with increased stereotypy. The effects of apomorphine on operant behavior appeared to depend on induced stereotypy, with rate-decreasing effects resulting from the disruption of ongoing behavior by stereotyped pecking aimed elsewhere in the chamber, and rate increases resulting from the redirection of elicited pecking towards the operant key.

Animals↗
PubMed1989

The effects of intrathecal administration of the dopamine agonist apomorphine on penile reflexes and copulation in the male rat.

Relatively high doses of systemically administered apomorphine inhibit penile reflexes. It is possible that these inhibitory effects are due, at least in part, to actions of apomorphine on the lumbosacral spinal cord. The present experiments examined this possibility by injecting apomorphine (10 and 50 micrograms/5.0 microliters vehicle) into the lumbosacral subarachnoid space through chronic, indwelling cannulae. Such injections impaired ex copula penile reflexes, slowed the rate of copulation, and decreased the number of intromissions preceding ejaculation. These results suggest that lumbosacral cord dopamine receptors may normally regulate male sexual performance.

Animals↗
PubMed1982

Role of globus pallidus GABA and opiate receptors in apomorphine circling in nigro-striatal lesioned rats.

The effect of lesioning the ipsilateral globus pallidus (GP) on apomorphine-induced circling in nigro-striatal lesioned rats was investigated. A GP electrolesion almost abolished circling whereas a kainic acid lesion partly antagonized circling. Drugs that affect GABA and opiate receptors were injected in GP through a cannula. Circling was antagonized by the GABA antagonists picrotoxin and bicuculline, the GABA agonist muscimol and by baclofen. Opiate receptor agonists including morphine, levorphanol, [D-Ala2, D-Leu5]-enkephalin and beta-endorphin had no effect on circling in GP. Ethylketazocine caused a pronounced, naloxone-reversible slowing of apomorphine circling. Apomorphine-induced circling behaviour may be modulated by GP GABA receptors and kappa-type opiate receptors.

Animals↗
PubMed1994

The ontogeny of apomorphine-induced alterations of neostriatal dopamine release: effects on potassium-evoked release.

The effects of apomorphine (0.05, 0.1, and 1.0 mg/kg, s.c.) on K(+)-evoked dopamine release were studied through the use of in vivo microdialysis in the neostriatum of developing and adult rats. Fifteen-minute samples were collected from urethane-anesthetized rats 5, 10-11, 21-22, 35-36 days of age, and adults, and quantified by high performance liquid chromatography with electrochemical detection. Apomorphine attenuated K(+)-evoked dopamine release in all age groups, suggesting that the dopamine autoreceptor modulating release in the neostriatum is functional by 5 days of age. A dose-response effect of apomorphine was observed in all age groups except at 5 and 10 days of age. Absolute levels of extracellular dopamine were significantly lower at 5 and 10 days of age compared with the other ages, and the effectiveness of a high-K+ artificial cerebrospinal fluid to evoke dopamine release increased with age.

Aging↗
PubMed1975

Electroconvulsive shock and postsynaptic catecholamine effects: increased psychomotor stimulant action of apomorphine and clonidine in reserpine pretreated mice by repeated ECS.

Male mice were administered electric convulsive shocks (ECS) once daily for one (ECS X I), three (ECS X III) or seven days (ECS X VII). One (day 1), three (day 3) or six days (day 6) later they received reserpine 10 mg/kg, followed 2 hours later by clonidine, 1.5 mg/kg, and/or apomorphine, 1.5 mg/kg. Control animals received the same drug treatments but no ECS. The motor activity was recorded for 1 hour, starting immediately after the last drug injection. The behavioral depression induced by reserpine was equally pronounced in ECS-pretreated animals as in the control animals. The psychomotor stimulant effects of clonidine and/or apomorphine, given after reserpine was, however, enhanced by pretreatment with ECS X VII, DAY 1. Pretreatment wit- ECS X VII increased the motor activity also in animals given reserpine, apomorphine and clonidine at day 3 or day 6. ECS X III was also effective in this respect at day 1, whereas ECS X I, day 1, was ineffective. Mice given ECS X VII but no drug treatment showed at day 1 an increased motor activity during the initial 10 min and a decreased activity during the last 10 of the 1 hour recording period. At day 3 and day 6 after ECS X VII the motor activity was increased in comparison to that in untreated control animals during the whole 1 hour period. Animals given repeated ECS furthermore showed increased irritability and reduced body weight. The results indicate that repeated ECS increase the sensitivity of postsynaptic catecholamine receptors in the brain or alter neuronal structures which are connected to these receptors.

Animals↗
PubMed1987

Lack of effects of apomorphine, haloperidol and clozapine on the synthesis and utilization of brain GABA.

The synthesis of GABA was studied as the accumulation of GABA following inhibition of the GABA-alpha-ketoglutaric acid aminotransferase by gamma-acetylenic GABA (GAG) or gamma-vinyl GABA. The disappearance of GABA was studied by means of inhibition of glutamate decarboxylase by 4-deoxypyridoxine. Systemic administration of the dopamine receptor agonist apomorphine did not change the accumulation or the disappearance of GABA in the substantia nigra and the corpus striatum of the rat. However, a very high dose of apomorphine somewhat increased the GAG-induced GABA accumulation in the corpus striatum. The dopamine receptor antagonists haloperidol and clozapine did not modify the accumulation and disappearance of GABA in the two structures, except for a slight decrease in the GAG-induced GABA accumulation in the substantia nigra. Following an acute hemisection, the neural connections between the substantia nigra and the corpus striatum are interrupted on one side of the brain. Apomorphine did not influence the accumulation or the disappearance of GABA in the substantia nigra and in the corpus striatum on the sectioned side of the brain. These results indicate that the synthesis and the utilization of GABA in the two structures studied are not influenced to any greater extent by changes in dopamine receptor activity.

Animals↗
PubMed1983

Action of apomorphine, bromocriptine and lergotrile on gamma-aminobutyric acid and acetylcholine release in nucleus accumbens and corpus striatum.

The effect of three dopamine agonists, apomorphine, bromocriptine and lergotrile, was tested on the release of gamma-aminobutyric acid, (GABA) and acetylcholine (ACh) from tissue slices of rat nucleus accumbens and striatum. All three agents in vitro caused a dose dependent depression of the K+-evoked release of [14C]-GABA in corpus striatum. This effect was also obtained following in vivo drug application and when endogenous GABA release was determined. A similar depression of GABA release was obtained in the nucleus accumbens. Both dopamine and dibutyryl adenosine-3':5'-cyclic monophosphoric acid inhibited the K+-evoked release of [14C]-GABA in corpus striatum. This inhibitory effect was not reversed by sulpiride. Bromocriptine and lergotrile also depressed the K+-evoked release of [3H]-acetylcholine from tissue slices of corpus striatum but not nucleus accumbens, as has previously been demonstrated for dopamine and apomorphine. In contrast, sulpiride enhanced the release of [3H]-acetylcholine and molindone reversed the apomorphine inhibition of [3H]-acetylcholine release. These results indicate that dopaminergic agents may influence the release of both GABA and ACh in the corpus striatum but only GABA in the nucleus accumbens.

Acetylcholine↗
PubMed1976

Apomorphine in the rat nucleus accumbens: effects on the synthesis of 5-hydroxytryptamine and noradrenaline, the motor activity and the body temperature.

Apomorphine (10 mug) was injected bilaterally into the nucleus accumbens or the neostriatum of rats. The application of apomorphine to the nucleus accumbens, but not to the neostriatum, enhanced the accumulation of 5-hydroxytryptophan in the central nervous system following inhibition of the aromatic L-amino acid decarboxylase. The effect was greatest in the brain stem particularly in the pons plus medulla oblongata. Similar but smaller rises were observed for the accumulation of DOPA in noradrenalinerich regions. The motor activity was increased and the body temperature was decreased by apomorphine in the nucleus accumbens, whereas smaller or no effects were obtained from the neostriatum.

Animals↗
PubMed1988

The effect of chronic lithium administration and withdrawal on locomotor activity and apomorphine-induced locomotor stimulation in rats.

The effect of chronic lithium administration and withdrawal on locomotor activity and apomorphine-induced locomotor stimulation in rats was studied. Chronic lithium administration caused a decrease in locomotor activity, which might be due to a lithium-induced decrease of exploratory behaviour. Chronic lithium administration had no effect on apomorphine-induced locomotor stimulation. However, apomorphine-induced locomotor stimulation was increased two days after the withdrawal of lithium while no difference was found after four days, suggesting a transient increase in postsynaptic dopamine (DA) receptor sensitivity following lithium withdrawal.

Animals↗
PubMed1992

Cardiovascular reflexes in Parkinson's disease: effect of domperidone and apomorphine.

Cardiovascular reflexes were evaluated in 18 patients with idiopathic Parkinson's disease who had a Hoehn & Yahr score of III-IV. The effect of apomorphine and domperidone on blood pressure, heart rate, R-R interval variation, and the Valsalva ratio were studied. Autonomic dysfunction was not found in the patients and there were no differences between subgroups of patients on different treatments. Apomorphine altered cardiovascular reflexes to a greater degree in patients who received the drug for the first time than in chronically treated patients. The changes were antagonized by domperidone, a peripheral dopamine receptor antagonist. Apomorphine treated patients who were receiving long-term domperidone had similar abnormalities of cardiovascular reflexes to those who had been able to withdraw it.

Aged↗
PubMed1988

Anatomical analysis of the involvement of mesolimbocortical dopamine in the locomotor stimulant actions of d-amphetamine and apomorphine.

Lesion studies employing 6-hydroxydopamine (6-OHDA) suggest that locomotor hyperactivity induced by certain stimulant drugs is dependent on dopaminergic neurotransmission in the nucleus accumbens (NACC). However, studies to date have not adequately controlled for the reported effects of 6-OHDA on baseline (non-drug) activity and on DA levels in other terminal regions. Slow bilateral infusions of 6-OHDA into the NACC, but not into olfactory tubercle (OT) or medial prefrontal cortex (mPFCx), reduced d-amphetamine (0.5 mg/kg SC) hyperactivity and resulted in a "supersensitive" (hyperactive) response to a low dose of apomorphine (0.1 mg/kg SC) in photocell cages. Direct observation revealed no behavioral changes in OT lesioned rats challenged with apomorphine which might correspond to a "denervation supersensitivity" syndrome. Assays of DA and 5-hydroxytryptamine (5-HT) in mPFCx, OT, NACC, and caudate-putamen revealed that 6-OHDA infusion into NACC caused substantial DA loss in NACC, OT and mPFCx, whereas infusion at mPFCx or OT sites depleted DA locally (greater than 85% loss) with little or no remote change. Concentrations of 5-HT were little altered by 6-OHDA, except for a local depletion in mPFCx. The present results confirm the importance of nucleus accumbens DA in the expression of locomotor stimulation induced by apomorphine and d-amphetamine, and suggest that the mPFCx and OT do not make an important contribution.

Animals↗
PubMed1988

Alpha 1- and alpha 2-adrenoreceptor antagonists differentially influence locomotor and stereotyped behaviour induced by d-amphetamine and apomorphine in the rat.

The importance of dopamine (DA) in mediating locomotor, exploratory and stereotyped behaviour in rodents is well established. Evidence also indicates a modulatory role for noradrenaline (NA) although, due to nonspecificity. of previously available agents, a precise role remains undefined. The effects of the specific and selective alpha-adrenoreceptor antagonists idazoxan (alpha 2) and prazosin (alpha 1) on behaviour induced by amphetamine and apomorphine have been investigated in the rat. d-Amphetamine (2 mg/kg) induced hyperactive locomotion and exploration. Pretreatment with prazosin (1 mg/kg) markedly reduced these responses. In contrast, pretreatment with idazoxan (20 mg/kg) only marginally altered d-amphetamine hyperactivity. Apomorphine (0.5 mg/kg) induced biphasic locomotor and exploratory activity. Neither alpha-antagonist affected the initial burst of activity (60 min), although prazosin inhibited whereas idazoxan potentiated the secondary phase (90-180 min). At higher dosage, amphetamine (6 mg/kg) and apomorphine (2 mg/kg) induced stereotyped behaviours. Prazosin pretreatment enhanced stereotyped gnawing and decreased sniffing and locomotion, whereas idazoxan increased locomotion and decreased amphetamine-induced mouth movements. These data indicate that DA-induced locomotor and stereotyped behaviours are differentially influenced (in opposite directions) by both alpha1- and alpha 2-adrenoreceptor antagonists. NA may thus modulate the expression and character of behaviour by influencing DA function in certain brain areas.

Adrenergic alpha-Antagonists↗