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PubMed1985

Sedation and sleep induced by high doses of apomorphine after blockade of D-1 receptors by SCH 23390.

The effect of SCH 23390, a selective blocker of D-1 receptors, on apomorphine-induced behavioural and EEG changes was studied in rats. In control rats, a low dose of apomorphine (50 micrograms/kg s.c.) produced sedation associated with EEG synchronization. A high dose of apomorphine (1 mg/kg s.c.) produced stereotypy associated with EEG desynchronization. At the dose of 1 mg/kg i.p., SCH 23390 decreased motor activity but failed to alter the EEG pattern. The administration of either the low or high dose of apomorphine to SCH 23390-treated rats elicited a marked sedative response associated with EEG synchronization. The EEG synchronization produced by apomorphine (50 micrograms/kg) in SCH 23390-treated rats was prevented by (-)-sulpiride (25 mg/kg i.p.), a D-2 receptor blocker. It is concluded that by preventing the excitatory response to apomorphine SCH 23390 discloses the existence of a population of D-2 receptors mediating sedation and sleep.

Animals↗
PubMed1990

The role of multiple dopamine receptors in apomorphine and N-n-propylnorapomorphine-induced climbing and hypothermia.

Apomorphine and N-n-propylnorapomorphine (NPA) were compared for their ability to induce stereotyped cage climbing and hypothermia in mice. Climbing behavior was produced by similar doses of apomorphine and NPA (0.625-2.5 mg/kg s.c.), whereas NPA was 43 times more potent than apomorphine in inducing a hypothermic response. SKF38393 caused a shift to the left in the dose-response curve for NPA-induced climbing, the ED50 changing from 0.98 to 0.014 mg/kg. SKF38393 had no effect on apomorphine-induced climbing behaviour. The climbing response produced by apomorphine was antagonised by both D-1 and D-2 antagonists. Climbing behaviour induced by NPA (2.5 mg/kg) could be antagonised by SCH23390 but not by clebopride, however climbing behaviour induced by a low dose of NPA (0.06 mg/kg) plus SKF38393 could be blocked by both D-1 and D-2 receptor antagonists. The hypothermic responses produced by either apomorphine or NPA could only be reversed by the selective D-2 antagonist, clebopride. These results demonstrate that dopamine agonist-induced stereotyped cage climbing requires both D-1 and D-2 receptor stimulation, whereas the hypothermic response is D-2-mediated. The results also show that it is possible to assess the relative activity of a dopamine agonist at D-1 or D-2 receptors in vivo by comparing the ability of the compound to induce hypothermia and climbing behaviour.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Effect of apomorphine on oxytocin concentrations in different brain areas and plasma of male rats.

The effect of the dopamine (DA) agonist, apomorphine, on oxytocin concentrations in the hypothalamus, hippocampus, septum and plasma was studied in male rats. Apomorphine dose dependently increased the concentration of oxytocin in the plasma and hippocampus, the minimal effective dose being 80 micrograms/kg s.c., which induced a 65% increase in plasma and a 45% increase in the hippocampus. The maximal effect (210 and 125% above controls) was induced with 240 micrograms/kg s.c. In contrast, there was a significant decrease (32%) in the oxytocin concentration in the hypothalamus, but only after the highest doses of apomorphine, while no change was found in the septum. The apomorphine effect in the hippocampus and hypothalamus was prevented by the mixed DA D-1/D-2 receptor blocker, haloperidol (0.3 mg/kg i.p.), and by the DA D-2 receptor blocker, (-)-sulpiride (20 mg/kg i.p.), but not by the DA D-1 receptor blocker, SCH 23390 (0.2 mg/kg s.c.). Similar effects were found in plasma, although SCH 23390 inhibited the apomorphine effect by 45%. Our results suggest that apomorphine stimulates oxytocinergic transmission in male rats and provide biochemical support for the hypothesis that a DA-oxytocin link exists in the central nervous system.

Animals↗
PubMed1992

Effects of cortical ablation on apomorphine- and scopolamine-induced changes in dopamine turnover and ascorbic acid catabolism in the rat striatum.

Levels of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), ascorbic acid and dehydroascorbic acid (DHAA) were measured by HPLC in the striatum of rats whose fronto-parietal cortex had been unilaterally ablated after a single injection of apomorphine (1 mg/kg s.c.), scopolamine (0.6 mg/kg s.c.) or L-glutamate (500 mg/kg i.p.). Unilateral cortical ablation decreased striatal levels of glutamate in both striata ipsilateral (35%) and contralateral (17-25%) to the lesion. Apomorphine and scopolamine significantly increased (+94 and +122%, respectively) the DHAA/ascorbic acid ratio in the striata ipsilateral to the lesion in unoperated and sham-operated rats (+72 and +34%, respectively), but both drugs failed to increase it in ablated rats. L-Glutamate significantly increased the DHAA/ascorbic acid ratio in unoperated (+53%) and ablated rats (+37%). The increase in sham-operated rats (+34%) did not reach statistical significance. Apomorphine and scopolamine significantly decreased the DOPAC/DA ratio in the striata ipsilateral to the lesion of unoperated, sham-operated and ablated rats. The decrease in the DOPAC/DA ratio induced by apomorphine and scopolamine was greater in ablated rats than in sham-operated rats. L-Glutamate induced only minor changes in striatal DA and DOPAC levels. We conclude that the apomorphine- and scopolamine-induced increase in ascorbic acid oxidation in the striatum requires intact cortico-striatal glutamatergic pathways. Cortical ablation potentiates the apomorphine- and scopolamine-induced inhibition of striatal DA turnover.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

A comparative study of the locomotor activity effects of apomorphine and the "atypical dopamine agonists" (piribedil and S3608).

Apomorphine and the "atypical dopamine agonists" (piribedil and S3608) dose dependently increase locomotor activity (LA) in rats. The LA effects of all 3 drugs are readily attenuated by pretreatment with pimozide or sulpiride. Reserpine pretreatment or bilateral 6-hydroxydopamine lesions of the nucleus accumbens (NAS) potentiates apomorphine-induced LA but attenuates piribedil- and S3608-induced LA. The latter suggests an indirect mode of action for piribedil and for S3608. However, piribedil and S3608 at concentrations up to 10(-4)M do not cause release or inhibition of 3H-dopamine uptake in synaptosomes prepared from the rat NAS. Sulpiride antagonism of apomorphine-induced LA is surmountable by increasing the dose of apomorphine. Antagonism of piribedil- or S3608-induced LA by sulpiride is not surmountable by increasing the dose of either of the "atypical dopamine agonists". Furthermore, pretreatment with either piribedil or S3608 substantially increases the peak LA inducible by apomorphine. The effects of simultaneous injections of piribedil and S3608 are, however, not additive. These findings suggest that the LA stimulant effects of piribedil and S3608 are mediated via receptors or systems which differ from the receptors involved in the mediation of apomorphine-induced LA.

Animals↗
PubMed1982

Non-opiate beta-endorphin fragments and dopamine--II. beta-Endorphin 2-9 enhances apomorphine-induced stereotypy following subcutaneous and intra-striatal injection.

The non-opiate beta-endorphin (beta E) fragment 2-16 (des Tyr1-alpha-endorphin) enhanced apomorphine-induced stereotyped sniffing in rats, but did not interfere with the hypoactivity elicited by small doses of apomorphine. Structure-activity relationship studies revealed that the active moiety of alpha-endorphin fragments with respect to their potentiating effects on apomorphine-induced stereotyped sniffing resides in the beta E fragment 2-9. Subsequent studies showed that the potentiating influence of beta E 2-9 was dependent on the dose of the peptide and that the interaction between this peptide and apomorphine may be non-competitive in nature. The stereotyped sniffing elicited by apomorphine, injected bilaterally into the striatal area of the brain, was dose-dependently enhanced by intra-striatal pretreatment with beta E 2-9. It is concluded that the influence of alpha-type endorphins and beta E 2-9 on apomorphine-induced behavioural changes, is in some aspects opposite to that of gamma-type endorphins, but may be mediated by quite different mechanisms.

Animals↗
PubMed1982

Antipodal central effects of apomorphine and dopamine in chickens.

Dopamine, infused into the hypothalamus or injected into the 3rd cerebral ventricle of chickens pretreated with mebanazine, induced behavioural and electrocortical sleep, suppressed motor activity and lowered body temperature and CO2 elimination, effects prevented by phenoxybenzamine but not spiperone. The hypothermic effects of dopamine were intensified by testing chicks below thermoneutrality. Ampomorphine, infused into the hypothalamus, injected into the 3rd cerebral ventricle or given intravenously, evoked behavioural and electrocortical arousal in the intact chicken and in the encéphale isolé preparation. Additionally, pecking, vocalization, increased motor activity and CO2 elimation were elicited; body temperature was elevated in about half the chickens but lowered in the remainder. Chicks tested below thermoneutrality responded with a fall in body temperature to apomorphine, the fall being greatest for those in which apomorphine had hypothermic actions at thermoneutrality. The actions of apomorphine, except on body temperature, were antagonized by spiperone. The effects of apomorphine resembled those of dexamphetamine, but whereas those of the latter were antagonized by less than equimolar dosage of methysergide, the effects of apomorphine were not; spiperone, effective against apomorphine, in equimolar dosage did not prevent the effects of dexamphetamine in 3 of 4 chickens tested.

Animals↗
PubMed1988

The response of apomorphine administered into the accumbens in rats with bilateral lesions of the nucleus accumbens, induced with 6-hydroxydopamine.

Bilateral lesions of the nucleus accumbens, induced with 6-hydroxydopamine, reduced motor activity and produced a 20-35% depletion of the concentrations of dopamine (DA) and its main metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Small doses of apomorphine (1-10 ng), injected into the nucleus accumbens of sham-lesioned rats, decreased motor activity, while larger doses (1-10 micrograms) produced hyperactivity. In rats lesioned with 6-hydroxydopamine, apomorphine caused hyperactivity only, and this apomorphine-induced response was more pronounced than in sham-lesioned rats. Large doses of apomorphine decreased, only in sham-lesioned animals, the levels of DOPAC and HVA. These data suggest that the apomorphine-induced hypomotility is mediated by presynaptically located DA receptor systems in the nucleus accumbens, whereas the apomorphine-induced hypermotility is likely to be mediated by postsynaptically located DA receptor systems.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Effects of intraperitoneal administration of apomorphine and the isomers of 3-(1-propyl-3-piperidinyl)phenol on the firing activity of substantia nigra dopamine neurons: comparison of agonist efficacies and development of acute tolerance.

The effects of intraperitoneal administration of apomorphine, (+)-3-PPP, and (-)-3-PPP on slow-(less than 4 spikes/sec) and fast-(greater than 4 spikes/sec) firing dopaminergic neurons in the substantia nigra zona compacta of rats anesthetized with chloral hydrate were assessed. All compounds completely inhibited slow-firing dopaminergic neurons. When a dose-response was determined by administering each dose in a single bolus injection, apomorphine and (+)-3-PPP produced dose-related inhibitions of fast-firing dopaminergic neurons, with the largest dose of each compound completely inhibiting nearly all cells tested. In contrast, (-)-3-PPP only partially inhibited (50%) fast-firing dopaminergic neurons. Thus, on fast-firing neurons, (-)-3-PPP had the profile of a partial agonist, while apomorphine and (+)-3-PPP demonstrated greater efficacy than (-)-3-PPP. Pretreatment while doses of apomorphine, (+)-3-PPP, or (-)-3-PPP that partially inhibited the activity of dopaminergic neurons antagonized the complete inhibitory effects of a dose of apomorphine that normally produced complete inhibition of neuronal firing. In addition, pretreatment with doses of (+)-3-PPP that partially inhibited the activity of cells antagonized the complete inhibitory effects of a dose of (+)-3-PPP that, normally produced complete inhibition of neuronal firing. From the antagonism studies alone, it was not clear if tachyphylaxis or partial agonist activity accounted for the observed antagonisms. However, since apomorphine and (+)-3-PPP completely inhibited the activity of fast-firing DA neurons, it is proposed that they antagonize by inducing a dose- and time-dependent tachyphylaxis. In contrast, (-)-3-PPP is proposed to antagonize by virtue of its partial agonist activity.

Action Potentials↗
PubMed1989

Blockade of apomorphine-induced yawning in rats by the dopamine autoreceptor antagonist (+)-AJ 76.

The effects of the putative, selective dopamine autoreceptor antagonist (+)-AJ 76 on yawning, penile grooming and mouth movements induced by small doses of apomorphine in male rats were examined. Yawning induced by 0.05mg/kg apomorphine was dose dependently blocked by (+)-AJ-76, significant decreases being observed at 0.86 and 3.5mg/kg of the drug. A dose of 0.86mg/kg (+)-AJ 76 caused a two fold shift to the right of the apomorphine dose response curve for yawning. In contrast, (+)-AJ 76 had no effect on penile grooming and vacuous mouth movements induced by small doses of apomorphine. This pattern of results is similar to that observed after bilateral 6-hydroxydopamine-induced lesions of the substantia nigra which also blocked apomorphine-induced yawning but spared penile grooming and mouth movements. Previous studies have suggested that (+)-AJ 76 is a selective dopamine autoreceptor antagonist that has little or no effect on behaviour mediated by post-synaptic dopamine receptors. Therefore, these data provide further support for the hypothesis that apomorphine-induced yawning is mediated by dopamine autoreceptors.

Animals↗
PubMed1991

The effects of apomorphine on the hippocampal field potential in freely moving rats: pharmacological evidence of the involvement of D2 receptors.

The effects of apomorphine on the hippocampal field potential of dentate granule cells were investigated in freely-moving male Sprague-Dawley rats. Five sequential field potentials were recorded from the dentate gyrus of the dorsal hippocampus, by stimulating the perforant path in the entorhinal cortex at 30 sec intervals. The slope of the population excitatory postsynaptic potential (EPSP) slope and the amplitude of the population spike of these field potentials were analyzed and averaged with a computer. The effects of apomorphine were observed at intervals of 15 min over 2 hr. Although the slope of the population EPSP showed no significant change after the administration of apomorphine (1.0 mg/kg, i.p.), the amplitude of the population spike was enhanced by about 30%. This enhancement continued for about 90 min. These results suggest that the apomorphine does not change the synaptic input from the perforant path to the granule cells but enhances the excitability of the hippocampal dentate granule cells. This effect of apomorphine on the amplitude of the population spike was decreased by sulpiride (20 mg/kg, i.p.) but was not affected by SCH-23390 (0.1 mg/kg, i.p.). These results lead to the conclusion that the enhancement of the excitability of the dentate granule cells by apomorphine is caused by the activation of the postsynaptic D2 receptors.

Animals↗
PubMed1995

Recovery of erectile function by the oral administration of apomorphine.

OBJECTIVES: Apomorphine has been reported to be effective in causing erections in animals and man when administered parenterally. The side effects, notably nausea, have seriously limited its clinical usefulness. We formulated apomorphine for controlled sublingual absorption and herein report on four preliminary studies evaluating efficacy and side effects in men with no documentable organic cause of erectile dysfunction. METHODS: Patients complaining of erectile dysfunction underwent a careful evaluation. Those with measurable organic dysfunction or known organic factors were excluded. Men with primarily psychogenic impotence were tested with one of four protocols of an apomorphine preparation (preliminary sublingual liquid, preliminary 5 mg tablet, aqueous nasal spray, and new 3 and 4 mg controlled absorption tablets). The erectile response of these men to the drug with visual erotic or sexually neutral stimulation was studied with the Rigiscan. RESULTS: Seven of 10 evaluable patients responded to the sublingual liquid preparation but the majority experienced significant nausea. The preliminary 5 mg tablet and aqueous forms did not produce useful responses free of side effects. The newly formulated controlled absorption 3 and 4 mg tablets were tested in 12 men. Eight of 12 (67%) developed erections in response to apomorphine. Erectile activity was seen during sexually neutral visual stimulation to a significantly greater extent than with placebo. Home trial use was found to be successful and sustained by 7 of 11 (64%) patients. CONCLUSIONS: We have shown that apomorphine will act as an erectogenic agent when absorbed through the oral mucosa. In a carefully selected group of impotent patients with no documentable organic causes of erectile dysfunction, but with proven erectile potential, 67% will experience significantly durable erections with a dose of 3 or 4 mg of apomorphine when formulated for controlled absorption. The results in these small groups appear to justify larger clinical studies of this proprietary formulation.

Administration, Sublingual↗
PubMed1984

Apomorphine effects on behavioral response to ethanol in mice selectively bred for differential sensitivity to ethanol.

Two lines of mice selectively bred for differences in response to a hypnotic dose of ethanol were administered apomorphine alone or in combination with ethanol. When administered by itself, apomorphine produced similar dose-dependent depression of locomotor activity and increases in stereotypy in the two lines. Doses of apomorphine (0.5 microM/kg and 2 microM/kg) thought to bind only presynaptic dopamine receptors blocked the slight locomotor activation to 1.5 g/kg ethanol in the ethanol-sensitive Long-Sleep (LS) mice; in the ethanol-insensitive Short-Sleep (SS) mice which show marked activation to all subhypnotic doses of ethanol, these doses of apomorphine only attenuated the activation. A higher apomorphine dose (8 microM/kg) antagonized the locomotor depressant effects of 2.0 and 2.5 g/kg of ethanol in LS mice but did not alter the shape of the SS ethanol dose response curve for locomotor activity. Apomorphine (2 and 8 microM/kg) potentiated ethanol-induced loss of the righting reflex in LS mice in a dose dependent fashion, but did not alter this soporific effect of ethanol in SS mice. These findings extend the data base suggesting a role for dopamine both in the mechanism(s) differentiating the LS and SS mice and the stimulant and intoxicating properties of ethanol.

Animals↗
PubMed1984

The effect of apomorphine on the open-field behavior of rats: alone and in pairs.

Male rats were observed in the open-field while alone and while in pairs in an alternating series of trials. The trials extended over a 78 min session following injections of either saline (0.9%) or apomorphine (5.0 mg/kg, IP) into the observed member of each pair. Contrary to the literature on apomorphine stereotypy, apomorphine did not induce continuous sniffing of the environment and continuous gnawing in most rats. Sniffing of the environment remained at normal levels but there was an increase in nodding the head in the vertical plane while keeping the snout close to the floor. Apomorphine-induced hyperactivity was attributed to two factors: a sustained increase in the duration of bouts of locomotion and a failure of the frequency of bouts of locomotion to habituate to novelty. Apomorphine eliminated all social behavior directed toward the other rat, however apomorphine rats showed they were sensible to the presence of the other by increasing their locomotion and rearing when the partner was introduced.

Animals↗
PubMed1984

Systematic comparison of apomorphine-induced behavioral changes in two mouse strains with inherited differences in brain dopamine receptors.

Dosage and time dependencies of apomorphine-induced changes in stereotyped behaviors (climbing, gnawing and sniffing), locomotor activity and rearing activity were compared in young adult male mice of two inbred strains, DBA/2 and C57BL/6. These two strains are known to differ in their genetically specified brain dopamine receptor number. Apomorphine administered intraperitoneally at dosages of 0.5-20 mg/kg failed to induced stereotyped climbing in DBA/2 at any of the doses tested but markedly increased climbing in C57BL/6 at higher dosages. Apomorphine-induced stereotyped gnawing occurred in both strains at higher dosages although the latency was shorter and maximal effect greater in C57BL/6. Stereotyped sniffing was induced in both strains to a comparable degree at doses greater than or equal to 2.0 mg/kg, and the duration of this stereotypy was indistinguishable between strains. Locomotor activity was inhibited maximally in DBA/2 at an apomorphine dosage of 2 mg/kg and was inhibited to a greater extent than was C57BL/6. Rearing was inhibited in both strains by doses of apomorphine greater than or equal to 0.5 mg/kg; however the duration of the effect was considerably greater in DBA/2 than in C57BL/6. These data suggest that genetically determined differences in central dopamine receptors may have profound and selective effects on behaviors mediated by dopamine pathways; that complex behavioral patterns, e.g., apomorphine-induced stereotypy, may be dissected in to individual components by identifying neuropharmaco genetic differences between strains; that marked strain-specific, inherited differences in dopamine agonist-induced behavioral changes do occur among inbred, non-mutant mouse strains and that their occurrence in other mammalian species including man should be considered.

Animals↗
PubMed1990

Apomorphine facilitates male sexual behavior of rhesus monkeys.

In the present study, a novel sexual behavior paradigm was used to study the effects of the dopamine agonist, apomorphine, on male sexual behavior of rhesus monkeys. In Experiment 1, the effects of apomorphine treatment were assessed by observing the behavioral responses of male rhesus to a sexually receptive female monkey that they could see, hear, and smell, but could not physically contact. Apomorphine treatment produced a spectrum of behavioral effects that differed depending on the dose of drug administered. Low doses of apomorphine (25-100 micrograms/kg) stimulated yawning, moderate doses (50-200 micrograms/kg) facilitated male sexual responses associated with the genitals including penile erection and masturbation, and high doses (greater than 200 micrograms/kg) elicited stereotypic behavior. Experiment 2 examined whether the behavioral responses of male monkeys to apomorphine treatment were influenced by the stimulus female. Apomorphine treatment facilitated penile erections in tests in which a stimulus female was present, but did not facilitate erections in tests in which she was absent. In sum, these experiments provide preliminary evidence that dopaminergic mechanisms may play a role in the regulation of male sexual behavior of rhesus monkeys.

Animals↗
PubMed1990

Omega-conotoxin prevents apomorphine- and oxytocin-induced penile erection and yawning in male rats.

The effect of the intracerebroventricular (ICV) administration of omega-conotoxin GVIA on penile erection and yawning induced by oxytocin or by the dopaminergic agonist apomorphine was studied in male rats. The peptide toxin, 1-10 ng given ICV 5 min before oxytocin (30 ng ICV) or apomorphine (80 micrograms/kg SC), but not its carboxymethylated (CM) derivative, prevented the above behavioral responses in a dose-dependent manner. Similarly, omega-conotoxin (5 ng) unilaterally injected in the paraventricular nucleus of the hypothalamus (PVN) prevented penile erection and yawning induced by the microinjection of oxytocin (10 ng) or apomorphine (50 ng) in the PVN. omega-Conotoxin injected in the PVN, but not in the preoptic area, prevented also penile erection and yawning induced by systemic apomorphine (80 micrograms/kg SC). ICV omega-conotoxin was unable to prevent stereotypy induced by apomorphine (500 micrograms/kg SC). The present results provide further evidence that calcium plays a major role in the expression of penile erection and yawning and that apomorphine and oxytocin induce these behavioral responses by mobilizing calcium through omega-conotoxin-sensitive (N-type) calcium channels.

Animals↗
PubMed1992

Effects of [D-Ala2, D-Leu5]enkephalin and [D-Pen2, L-Pen5]enkephalin on apomorphine-induced motor activity in the mouse.

The effects of intracerebroventricular injections of opioid peptides such as DADL [( D-Ala2, D-Leu5]enkephalin) and DPLPE [( D-Pen2, L-Pen5]enkephalin) with different degrees of selectivity for delta- over mu-receptor on apomorphine (0.1, 0.3, 1.0 and/or 3.0 mg/kg)-induced motor activity were investigated in the mouse using multi-dimensional behavioral analyses. Lower doses (0.1 and 0.3 mg/kg) of apomorphine failed to affect significantly motor activity, whilst higher doses (1.0 and 3.0 mg/kg) of the drug produced a marked increase in linear locomotion, circling, rearing, and/or grooming behaviors. DADL (0.03, 0.1 or 0.3 microgram) by itself did not influence behaviors, while the peptide (0.1 and 0.3 microgram) produced a marked inhibition on apomorphine (1.0 but not 3.0 mg/kg)-induced increase in rearing behaviors. Furthermore, the inhibitory effect of DADL (0.3 micrograms) on the apomorphine (1.0 mg/kg)-induced increase in rearing was reversed by treatment with the alkylating agent beta-FNA (beta-funaltrexamine) (5.0 micrograms). In contrast to the effects of DADL, the much more delta-selective opioid agonist DPLPE (0.3, 1.0 or 1.75 micrograms) had no marked effects on apomorphine (1.0 mg/kg)-induced behaviors. These results suggest that delta opioid receptors do not play a principal role in the apomorphine-induced increase in circling, rearing or grooming behaviors.

Analgesics↗