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PubMed1980

Psychopharmacological effects of low and high doses of apomorphine during ontogeny.

The effects of low (0.05 and 0.1 mg/kg) and high (1.0 and 3.0 mg/kg) doses of apomorphine on locomotor activities and stereotypies of 7, 14, 21, 28 and 35 day old rats were measured using a behavioral time-sampling procedure. High doses of apomorphine induced increases in matrix crossings and locomomtor movements at all ages tested. Apomorphine also induced wall climbing behavior in 7 and 14 day olds, but not older animals. A low dose suppression of activity was not seen until beginning at 28 days after birth using matrix crossings as a response measure, or at 35 days after birth using locomotor movements as a response measure. Stereotyped sniffing was not significantly increased by apomorphine until 21 days after birth and thereafter. Results are discussed in terms of differential maturation of dopamine auto- and postsynaptic receptors.

Age Factors↗
PubMed1981

Gastric relaxation and vomiting by apomorphine, morphine and fentanyl in the conscious dog.

Apomorphine (0.03 mg . kg-1 s.c.) and morphine (0.5 mg . kg-1 s.c.) produced gastric relaxation and vomiting in the conscious dog. Domperidone (0.1-1 mg . kg-1 i.v.), haloperidol (0.1 mg . kg-1 i.v.) and pimozide (0.025 mg . kg-1 i.v.) selectively blocked the gastric relaxation as well as the vomiting caused by apomorphine. Naloxone (0.07 mg . kg-1 i.v.) selectively blocked the gastric relaxation and the vomiting caused by morphine; after naloxone, morphine produced a delayed gastric relaxation in 2 experiments out of 7. These results suggest that for gastric relaxation as well as for vomiting, apomorphine and morphine act on different receptors. Fentanyl elicited marked gastric relaxation, blocked by naloxone, but did not elicit vomiting. After fentanyl, morphine and apomorphine no longer produced gastric relaxation and vomiting. This observation shows that the known blocking effect of fentanyl at the vomiting center does not affect its gastric relaxing effect.

Animals↗
PubMed1982

Snout contact fixation, climbing and gnawing during apomorphine stereotypy in rats from two substrains.

Apomorphine, at doses greater than or equal to 10 mg/kg (intraperitoneally), produced two patterns of stereotypy. In rats from one supplier it induced predominantly gnawing while in those from another predominantly climbing, suggesting that the response to the drug is influenced by genetic and/or experimental factors. At lower doses, apomorphine induced climbing in both groups (ED50 = 1.4 mg/kg in each group) but oral behavior in only one of them (ED50 = 1.3 mg/kg in one, and 8 mg/kg in the second group). Thus, at a given dose of apomorphine, different patterns of stereotypy may result from an interaction between two phenomena: the relative setting of the thresholds to mouth and to climb, and an inverse relation between oral activity and climbing. Analysis of climbing suggests that this response is comprised of two (previously unidentified) fundamental effects of apomorphine: snout contact fixation and bodywise forward progression.

Animals↗
PubMed1982

The persistence of hyperresponsiveness to apomorphine in rats following REM sleep deprivation and the influence of housing conditions.

The hyperresponsiveness to apomorphine disappears after REM sleep deprivation of rats; the time course of the disappearance was investigated. When REM sleep-deprived (REMd) rats were caged individually during the recovery period the increase in ambulation and in stereotyped behaviour elicited by apomorphine subsided within 8-24 h; on the other hand, the exaggerated aggressiveness persisted up to 64 days. However, when the deprived rats were allowed to recovery in groups of 3 per cage the increase in aggressiveness subsided after 4 days. Since individual housing of non-deprived rats for 4--11 days increased the apomorphine-aggressiveness steadily, 'isolation' probably summed with REM deprivation in facilitating the effects of apomorphine on aggressive behaviour. The results also suggest that the dopaminergic systems implicated in aggressive behaviour are sensitized by REM deprivation for a longer period than those subjacent to ambulation and stereotype.

Aggression↗
PubMed1982

Cycloheximide prevents apomorphine-induced yawning, penile erection and genital grooming in rats.

Apomorphine (50 micrograms/kg) induced repeated episodes of yawning, penile erection and genital grooming in rats. A dose of cycloheximide, which inhibited brain protein synthesis by 50% totally prevented apomorphine-induced yawning and reduced by approximately 50% the occurrence of episodes of penile erection and genital grooming. However, this treatment failed to modify the stereotyped behaviour induced by 200 micrograms/kg of apomorphine. These results suggest that protein synthesis is required for the behavioural effects of small doses of apomorphine.

Animals↗
PubMed1984

Effects of apomorphine on the in vivo release of dopamine and its metabolites, studied by brain dialysis.

The effect of apomorphine (0.05-0.5 mg/kg s.c.) on the release of endogenous dopamine and extracellular levels of the metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5HIAA) were examined in vivo by intracerebral dialysis. A dialysis tube was implanted stereotaxically through both caudate nuclei of rats and perfused with Ringer solution at a rate of 2 microliters/min. The amount of dopamine, DOPAC, HVA and 5HIAA in the perfusates was measured by HPLC with electrochemical detection. With the dialysis tube implanted into the striatum of anaesthetized rats it was possible to measure basal levels of dopamine and the metabolites in the perfusates; dopamine, 0.27 +/- 0.05 pmol/20 min (n = 15), DOPAC 43.3 +/- 2.57 pmol/20 min (n = 15), HVA 24.5 +/- 1.89 pmol/20 min (n = 15) and 5HIAA 13.9 +/- 1.77 pmol/20 min (n = 15). The % recoveries of the monoamines through the membrane were estimated to be 12% (dopamine), 21% (DOPAC), 23% (HVA) and 25% (5HIAA). Apomorphine 0.05-0.2 mg/kg decreased the spontaneous release of dopamine by a maximum of approximately 50%. When the dose of apomorphine was raised up to 0.5 mg/kg there was a 100% inhibition of dopamine release. Also, the extracellular levels of the metabolites DOPAC and HVA decreased following apomorphine administration; however there was no consistent change in 5HIAA. These findings indicate that the dopamine autoreceptors decrease dopamine release in vivo by 0-50% while larger decreases probably involve postsynaptic neurons engaging short- as well as long-loop reflexes.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Assessment of dopamine autoreceptor agonist properties of apomorphine, (+)-3-PPP and (-)-3-PPP by recording of yawning behaviour in rats.

Yawning behaviour in rats was studied by direct observation. Apomorphine dose dependently induced yawning: 0.05 mg/kg was most effective, 0.2 mg/kg induced locomotor and sniffing behaviour but less yawning. Sulpinide (2 and 10 mg/kg) dose dependently blocked the apomorphine (0.05 mg/kg)-induced yawning. (+)-3-PPP (1-10 mg/kg) induced yawning in a manner similar to that of apomorphine but (-)-3-PPP (1-10 mg/kg) did so only weakly. Yawning induced by (+)-3-PPP was blocked by sulpiride 10 mg/kg. It is concluded that (+)-3-PPP but not (-)-3-PPP is at least as effective as apomorphine to induce yawning in rats, indicating that (+)-3-PPP, but not (-)-3-PPP, is a pure agonist on dopamine autoreceptors.

Animals↗
PubMed1986

SCH 23390 antagonizes apomorphine- and ergot-induced hypothermia.

The reportedly specific D-1 dopamine (DA) receptor antagonist SCH 23390 significantly reduced the hypothermia elicited by various DA receptor agonists like apomorphine, pergolide and lisuride. When tested against equihypothermic doses of each agonist, SCH 23390 significantly reduced the hypothermia elicited by apomorphine (0.2 mg/kg s.c.) and by pergolide (0.1 mg/kg i.p.) at doses of 0.025 mg/kg s.c. Doses of 0.050 mg/kg s.c. of SCH 23390 were necessary to reduce the hypothermia elicited by 0.012 mg/kg s.c. of lisuride. Pretreatment with the specific D-2 antagonist (-)sulpiride (50 mg/kg i.p.) completely prevented the hypothermia elicited by lisuride (0.012 mg/kg i.p.), pergolide (0.1 mg/kg i.p.) and apomorphine (0.2 mg/kg s.c.) and shifted to the right the dose-response curve for agonist-induced hypothermia. A study of the interaction between 0.05 mg/kg s.c. of SCH 23390 with various doses of the agonists showed that the effectiveness of SCH 23390 in antagonizing the hypothermia was maximal towards apomorphine and least towards lisuride for which significant antagonism was observed only against the lowest dose tested (0.012 mg/kg s.c.). The reportedly specific D-1 receptor agonist SKF 38393 given in doses up to 20 mg/kg i.p. or intracerebroventricularly up to 100 micrograms failed to influence body temperature while it evoked intense grooming and stimulated motility.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

Apomorphine does not decrease tissue levels of tetrahydrobiopterin in vivo.

It was reported that R(-)apomorphine and other catechols are potent inhibitors of dihydropteridine reductase in vitro. It was suggested that decreased levels of tetrahydrobiopterin may represent a mechanism by which R(-)apomorphine inhibits catecholamine synthesis in vivo. This paper demonstrates that tetrahydrobiopterin levels are not affected either in vitro (PC12 cells) or in vivo (rat liver and corpus striatum) by treatment with R(-)apomorphine, whereas DOPA (3,4-dihydroxyphenylalanine) production (PC12 cells, corpus striatum) is reduced. This indicates that R(-)apomorphine does not inhibit DOPA production by reducing 6(R)-L-erythro-tetrahydrobiopterin) levels.

Animals↗
PubMed1987

The hypomotility elicited by small doses of apomorphine seems exclusively mediated by dopaminergic systems in the nucleus accumbens.

The reduction of motor activity elicited in rats by a subcutaneous injection of a small dose of apomorphine was reversed by pretreatment of the nucleus accumbens with haloperidol (10 pg), sulpiride (10 pg) or desenkephalin-gamma-endorphin (DE gamma E) (100 pg or 10 ng). These doses of the compounds did not change motor activity in placebo-treated rats. Pretreatment of the nucleus caudatus with the same neuroleptics or DE gamma E did not diminish the effect of subcutaneously administered low doses of apomorphine. A small dose of apomorphine decreased motor activity when it was injected directly into the nucleus accumbens. This effect was dose dependently antagonized by subcutaneous pretreatment with DE gamma E. It is suggested that the hypoactivity elicited by small doses of apomorphine is exclusively mediated by dopaminergic systems in the nucleus accumbens.

Analysis of Variance↗
PubMed1987

Cholecystokinin facilitates ejaculation in male rats: blockade with proglumide and apomorphine.

Systemic administration of the active, sulfated form of cholecystokinin-octapeptide (CCK-8S), at a dose known to inhibit dopamine (DA) release, significantly reduced the latency to ejaculate and number of intromissions preceding ejaculation in sexually active male rats. This effect was identical to that reported for low doses of the DA receptor agonist apomorphine, which bind preferentially to presynaptic DA autoreceptors. The facilitatory effect of CCK-8S on ejaculation was blocked by the putative CCK receptor antagonist proglumide and by a presynaptic dose of apomorphine. Blockade of the effect of CCK-8S with a presynaptic dose of apomorphine is consistent with CCK induction of depolarization block in DA neurons. These data suggest that CCK-8S and apomorphine may reduce the ejaculation threshold in sexually active male rats by inhibition of DA release via two different mechanisms of action.

Animals↗
PubMed1987

Dopaminergic control of the cough reflex as demonstrated by the effects of apomorphine.

The effect of apomorphine on the cough reflex induced by electrical stimulation of the superior laryngeal nerve was studied in cats anesthetized with pentobarbital. Intravenous administration of apomorphine in doses which ranged from 0.1 to 1.0 mg/kg decreased the number of coughs in a dose-dependent manner. Haloperidol (0.3 mg/kg i.v.) did not significantly change the number of coughs. However, haloperidol administered 15 min prior to administration of apomorphine abolished the apomorphine-induced decrease in the number of coughs. These results suggest that dopaminergic mechanisms could have an important role in the regulation of the cough reflex.

Animals↗
PubMed1987

Prevention of amphetamine-induced behavioral hypersensitivity by concomitant treatment with microgram doses of apomorphine.

Behavioral hypersensitivity induced by subchronic administration of amphetamine in mice was inhibited by concomitant administration of apomorphine in microgram doses. Acutely, amphetamine followed in 15 min by apomorphine, produces a normal rise in locomotor activity subsequent to the action of amphetamine and an inhibition of that activity by the modulatory action of apomorphine. We suggest that apomorphine acts at a presynaptic neuronal site to interrupt the process(es) responsible for the development of stimulant-induced sensitization.

Amphetamine↗
PubMed1988

Increased grooming behaviour is induced by apomorphine in mice treated with discriminant benzamide derivatives.

Grooming behaviour in mice was dose dependently increased by SK&F 38393 (1.87-30 mg/kg), whereas it was dose dependently decreased by RU 24926 (2.5-10 mg/kg) or LY 171555 (0.4-1.6 mg/kg) alone or combined with SK&F 38393 or apomorphine (0.39-6 mg/kg). The inhibitory effect of 0.75 mg/kg apomorphine on grooming behaviour was not modified by SCH 23390, chlorpromazine, clozapine and thioridazine. In contrast, it was antagonized by eight other dopamine antagonists: a partial restoration to grooming scores lower or similar to those determined in control mice was obtained with flupentixol, haloperidol, metoclopramide, thioproperazine and tiapride, whereas a reversal to grooming scores higher than those determined in control mice was obtained with mice treated with (+/-)-sulpiride, amisulpride or RIV 2093. Furthermore, only SCH 23390, chlorpromazine and clozapine antagonized SK&F 38393 (1.87 mg/kg)-induced grooming behaviour, whereas the effects of flupentixol, thioridazine, metoclopramide, haloperidol and amisulpride in SK&F 38393-treated mice were parallel to those of control mice. Finally, SCH 23390 (20 micrograms/kg) antagonized the apomorphine-induced grooming in mice treated with amisulpride, (+/-)-sulpiride or tiapride. These data confirm the potential role of D-1 dopamine receptors in the expression of grooming behaviour and indicate that the dopamine receptors involved in the inhibition of grooming could be of the D-4 subtype. Our results also reveal that chlorpromazine and clozapine have D-1 antagonist properties and suggest that the modulation of apomorphine-induced grooming behaviour by dopamine antagonists in mice could be used as a test for their classification according to their activity at the different dopamine receptor subtypes.

Animals↗
PubMed1989

Apomorphine potentiates vagal bradycardia.

The effects of apomorphine, a dopamine (DA) agonist, on vagal bradycardia were investigated in chloralose-anesthetized dogs. Negative chronotropic responses to vagal nerve stimulation were significantly potentiated by apomorphine (10, 20 or 200 micrograms/kg i.v.). Pretreatment with the non-selective DA antagonist, haloperidol, or the selective DA2 antagonist, domperidone (but not the selective DA1 antagonist, SCH 23390), antagonized the effect of apomorphine. These results demonstrate that apomorphine potentiates electrically induced vagal bradycardia by a specific action on DA2 receptors which could be located on vagal nerve endings.

Anesthesia↗
PubMed1990

Dopamine D-1 but not D-2 receptor stimulation of the dorsal striatum potentiates apomorphine-induced jaw movements in rats.

The effects of bilateral injections of selective D-1 and D-2 agonists and antagonists into the dorsal striata on apomorphine-induced jaw movements were studied in ketamine-anaesthetized rats after C1 spinal transection. A phototransducer attached to the lower mandible automatically detected jaw movements. YM-09151-2 (0.2 and 0.5 micrograms) and cis(Z)-flupentixol (0.5 and 1 microgram) injected into the dorsal striatum increased the frequency of jaw movements after apomorphine (0.2 mg/kg i.v.). The effects were prevented by administration of SCH23390 (1 microgram) with YM-09151-2 (0.5 microgram) or cis(Z)-flupentixol (1 microgram). Injection of SCH23390 (1 microgram) alone into the dorsal striatum failed to alter the apomorphine (0.5 mg/kg i.v.)-induced jaw movements. Local application of the selective D-1 agonists, SKF38393 (5 micrograms) and SKF75670 (10 micrograms), into the dorsal striatum potentiated the apomorphine (0.2 mg/kg i.v.)-induced jaw movements, while a D-2 agonist, quinpirole (10 micrograms), injected into the same site attenuated these movements. These data are suggestive of an oppositional D-1: D-2 receptor interaction in the dorsal striatum.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Sigma receptor binding affinity and inhibition of apomorphine-induced climbing.

Several relatively selective compounds with affinity for the sigma binding site were assessed for their ability to inhibit apomorphine-induced climbing in the mouse. Although, the majority of compounds inhibited apomorphine-induced climbing, there was no correlation between the ability to inhibit climbing and potency in sigma binding assays using [3H]1,3-di-o-tolylguanidine (DTG) or [3H](+)-pentazocine as ligands. The potency of the compounds to inhibit binding to muscarinic M1 or M2 receptors correlated with the potency to inhibit apomorphine-induced climbing. However, several of the compounds that inhibit climbing had microM affinity at muscarinic receptors. Whether these concentrations were achieved in vivo is unclear. Our data suggest that sigma activity per se is not responsible for inhibition of apomorphine-induced climbing.

Animals↗
PubMed1993

The development of behavioral sensitization to apomorphine is blocked by MK-801.

The effects of the non-competitive NMDA receptor antagonist, MK-801 (dizocilpine), on the development of sensitization to the mixed dopamine receptor agonist, apomorphine were examined. Rats pretreated with MK-801 (0.25 mg/kg) prior to 2.0 mg/kg apomorphine failed to show a progressive sensitization to the activating effect of apomorphine across six preexposure sessions, nor did they show enhanced activity relative to control rats in response to 0.5 mg/kg apomorphine, given alone, during a subsequent test for sensitization. These results support the view that MK-801 interferes with long-term neural changes underlying sensitization to stimulant drugs.

Animals↗