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At least 19 recordsLinked to original sources
PubMed1986

Reversal of supersensitive apomorphine-induced rotational behavior in mice by continuous exposure to apomorphine.

Mice with unilateral lesions of the nigrostriatal dopaminergic neurons, induced by an intrastriatal injection of 6-hydroxydopamine, respond to an acute injection of apomorphine by rotating in a direction contralateral to the lesion. The dose of apomorphine that produced a half-maximal turning response was 0.4 mumol/kg s.c.; maximal turning responses were seen at 2 mumol/kg s.c. This behavioral supersensitivity may be due to an increased density of dopaminergic receptors. To determine whether continuous stimulation of these receptors with a dopaminergic agonist would reverse the dopaminergic behavioral supersensitivity, mice were exposed to continuous infusion of apomorphine via a s.c. implanted osmotic minipump containing 150 mumol of apomorphine in 0.2 ml and then challenged with an acute injection of apomorphine (2 mumol/kg s.c.) at varying times after the implant. Initially, the mice displayed spontaneous rotational behavior beginning by 1 hr after implantation, but this spontaneous behavior diminished over time and was absent by 4 days after implantation. The turning response of mice challenged with an acute injection of apomorphine was significantly reduced at 1 day after the chronic implantation and was totally absent at 2 and 4 days after implantation. This effect of continuous exposure to apomorphine was found to be concentration- and time-dependent; mice implanted with pumps containing 75 mumol of apomorphine required 8 days of exposure for tolerance to develop. Upon removal of the apomorphine-containing implants, the supersensitive rotational behavior returned over a 7-day period, with 50% recovery occurring at 2 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Time-course of apomorphine in the brain of the immature rat after apomorphine injection.

The time-course of apomorphine in brain was studied in 7-day-old and young adult rats following i.p. injection of 10 mg/kg apomorphine. In the adult animals continuous stereotypes behaviour (SB) commenced within 1-2 min and was no longer present at 75 min. The peak concentration of apomorphine was present at 5 min and then declined exponentially (half-life = 10.5 min); only trace amounts (less than 0.01 mug/g) were present at 90 min. In the immature rat apomorphine induced an initial phase of intermittent locomotion lasting about 10 min after which the rats appeared sedated; 60-80 min after injection intermittent SB emerged and terminated 150-180 min after the apomorphine injection. The peak brain concentration of apomorphine was present at 10 min and then declined exponentially (half-life = 28 min). Significant amounts of apomorphine were still present in brain at 150 min and trace amounts evident at 180 min. The reason for the delayed onset of SB in the immature rat is unclear. The longer half-life is presumably related to incomplete development of enzyme systems metabolizing apomorphine in the immature animal.

Animals↗
PubMed1989

Effects of repeated apomorphine and haloperidol treatments on subsequent behavioral sensitivity to apomorphine.

In a 2 x 2 factorial design, four groups of rats (n = 10 each) were injected daily with haloperidol (0.5 mg/kg IP) or its injection vehicle and apomorphine (1.0 mg/kg SC) or its vehicle for 21 consecutive days. Then, following a six-day drug-free rest interval, all rats were tested for locomotor activity in photocell arenas after an apomorphine injection on four additional days. Major findings were as follows: (a) rats pretreated with apomorphine were significantly more active following an apomorphine injection than rats pretreated with vehicle; (b) the development of sensitization to apomorphine was completely blocked by the concurrent administration of haloperidol during the pretreatment phase; and (c) pretreatment of rats with haloperidol alone did not affect subsequent sensitivity to apomorphine. These results suggest that the development of behavioral sensitization to apomorphine is related specifically to the stimulation of dopamine receptors.

Animals↗
PubMed1978

Effects of apomorphine and apomorphine-L-dopa-carbidopa on alcohol post-intoxication symptoms.

In a randomised double-blind clinical trial on 58 gamma-alcoholics, the effect of apomorphine given orally in individual subemetic doses was compared with apomorphine-L-dopa-carbidopa and with placebo. No positive effects of treatment with apomorphine, or with the combination apomorphine-L-dopa-carbidopa, on alcohol consumption or post-intoxication symptoms could be demonstrated. In the group which received the combination apomorphine-L-dopa-carbidopa, the post-intoxication symptoms lasted significantly longer than in the other two groups.

Adult↗
PubMed1978

Apomorphine stereotypies and transmitter mechanisms in the striatum. I. Changes in the apomorphine stereotypies caused by drugs acting on the GABA-ergic, dopaminergic and cholinergic transmission.

Experiments on male albino mice were carried out in order to determine the effects of drugs connecting with the GABA-ergic, dopaminergic and cholinergic transmission, on apomorphine stereotypies. The agents acting on GABA-ergic transmission are found to reduce the intensity of apomorphine stereotypies in the following order (arranged from strongest to weakest effect and expressed in doses of microgram per mouse: GABA (100), aminooxyacetic acid (5), diazepam (20), picrotoxin (1), GABA (10), semicarbazide (30), picrotoxin (0.1). The agents acting on the dopaminergic transmission also reduce apomorphine stereotypies in the following order: haloperidol (20;2), L-DOPA (500 mg/kg, i. p.), alpha-methylparatyrosine (150 mg/kg, i. p.) diethyldithiocarbamate (200). The strongest antagonistic effect in the two groups of agents studied was found for haloperidol. The agents acting on the cholinergic transmission (agonists and antagonists of muscarinic and nicotinic cholinoreceptors) have no significant effect on apomorphine stereotypies. It is assumed that the striatum is not the only brain structure responsible for apomorphine stereotypies.

Aminooxyacetic Acid↗
PubMed1977

Subcutaneous injections of apomorphine, stimulus generalization and conditioning: serious pitfalls for the examiner using apomorphine as a tool.

This report shows that stimulus generalization occurs in rats conditioned by a single injection of apomorphine. The data suggest that apomorphine initially acts as an unconditioned stimulus (UCS) of an unconditioned response (UCR) that, in turn, produces stimuli which become conditioned stimuli (CS) of a conditioned response (CR) having a nature identical to that of the UCR. The study also shows that behaviour elicited by a subcutaneous injection of apomorphine depends on the part of the body selected for administration. The mentioned properties should be taken into account when apomorphine is used as a tool in studies on brain and behaviour.

Animals↗
PubMed1977

[Effects of hypothalamus and globus pallidus lesions and of apomorphine injections into the globus pallidus, caudate nucleus, substantia nigra and septum on the aggressive behavior induced by apomorphine treatment of rats (author's transl)].

Intraspecific apomorphine-induced aggressive behavior in the rat was not affected following electrolytic lesions of the ventromedial hypothalamus. Some inhibition of the aggressive behavior was found after lateral lesions and an almost total suppression after destruction of globus pallidus. These results, as well as those following localized injections of apomorphine into the septum, substantia nigra, caudate nucleus, and globus pallidus suggested that the latter anatomical region may be the major site of the action of apomorphine in the behavior studies. The role of acetylcholine is discussed.

Aggression↗
PubMed1976

[Aggressive behaviour induced by apomorphine: relations with some elements of the behavioural profile and with the sensitivity to apomorphine (author's transl)].

Aggressive rats could be differentiated from non-aggressive rats on a lower rate of rearing reactions in the open-field activity, as well as on a weaker aptitude for learning, increasing with the complication of the test. The two groups of rats had comparable activity, and a comparable response to pain. Apomorphine decreased the number of rearing reactions and defecations on open-field activity in the same manner in non-aggressive rats as in aggressive animals. In the usual housing conditions, apomorphine increased similarly locomotor activity in both groups, but in observation cages of "emotional" type, the increase was much more pronounced in aggressive rats than in non-aggressive animals.

Aggression↗
PubMed1985

Effects of multiple pretreatment with apomorphine and amphetamine on amphetamine-induced locomotor activity and its inhibition by apomorphine.

Mice were given a saline preinjection and habituation to the testing environment followed by injection of amphetamine (0.675-5.0 mg/kg IP) and apomorphine (AP, 15-80 micrograms/kg SC) 15 min later. AP produced a dose-dependent inhibition of the amphetamine-induced locomotor activity. A dose of 40 micrograms/kg AP increased approximately threefold the amphetamine dose required to induce the same increase in activity. Repeated administration of AP (30 mg/kg IP once daily for 14 days) resulted in an enhanced response (in the early portion of the time response) to amphetamine challenge, while the ability of subsequent microgram challenge doses of AP to reduce the response were unaffected. Similarly, repeated administration (twice-daily IP injections for 5 days) of amphetamine (5.0 mg/kg) resulted in an enhanced locomotor response to amphetamine challenge and no change in the ability of AP to inhibit the response. These results suggest that repeated administrations of dopamine agonists, although acting through different mechanisms (i.e., indirect versus direct), increase the initial release of neurotransmitter. However, the repeated administration of these agonists does not attenuate the ability of AP to inhibit the release of the neurotransmitter induced by amphetamine. The regulatory functions (i.e., presynaptic receptor control) of release appears to remain intact, but the level of neuronal activity has been increased.

Amphetamine↗
PubMedDate not supplied

Effects of some antidepressant drugs on apomorphine concentration in the central nervous system of rats and apomorphine-induced stereotypy.

Pharmacokinetic aspects of interaction between antidepressant drugs (AD) and apomorphine (APO) have been studied. It was found that neither acute nor chronic AD pretreatment affected the distribution of APO-induced stereotypy was not changed. An exception was citalopram (CIT) which given in a single dose to rats significantly potentiated APO-induced gnawing. Single dose of investigated AD delayed the onset of APO-induced sniffing, licking and gnawing, however the overall effect did not reach the statistically significant level. The presented results suggest that changes of APO behavioral effects induced by AD pretreatment are rather due to pharmacodynamic and not pharmacokinetic interaction.

Amitriptyline↗
PubMed1986

Disposition of apomorphine in rat brain areas: relationship to stereotypy.

Apomorphine-induced stereotyped behavior and apomorphine levels in plasma, striatum and nucleus accumbens were determined in rats at various intervals after a single i.p. injection of serial doses of apomorphine hydrochloride (0.625, 1.25, 2.5 and 5 mg/kg). Apomorphine disappeared from plasma in a mono-exponential mode with a half-life of about 10 min. In striatum and nucleus accumbens apomorphine concentrations peaked 10 min after administration, declining thereafter with a half-life comparable to that in plasma. Apomorphine was concentrated and distributed similarly in the two brain regions; the brain areas/plasma ratio was approximately seven for all doses tested. The rise of apomorphine levels in brain areas slightly preceded the behavioral response, whereas after the peak effect (20-30 min) the intensity of stereotypy declined almost parallel with the log drug concentrations. Plotting apomorphine levels in the tissues assayed against the drug response at the same interval for individual rats, regardless of dose, indicated a highly significant relation between the degree of behavioral effects and brain apomorphine levels. The threshold apomorphine concentrations for inducing stereotyped behaviour were 108 and 95 ng/g respectively in striatum and nucleus accumbens. These findings show that the time course and magnitude of the behavioral effects of apomorphine corresponded with its brain levels in 'dopaminergic' areas, suggesting that apomorphine-induced stereotyped behavior in rats can be described by a direct mechanism. Reserpine (5 mg/kg s.c.) enhanced the apomorphine stereotypy but did not affect apomorphine's disposition in brain and plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Evidence that the stimulus properties of apomorphine are mediated by both D1 and D2 receptor activation.

Male and female rats were trained to discriminate between the stimulus properties of apomorphine (0.16 mg/kg i.p.) and saline in a two-lever, food-motivated operant procedure. Apomorphine, at doses different than the training dose, produced a similar dose-dependent relationship in both sexes. Consistent with the hypothesis that the behavioral effects of apomorphine are mediated by D2 activation, the apomorphine interoceptive cue generalized to bromocriptine, a drug considered to be a preferential D2 agonist. In addition, the dose-response curve after 5-15 mg/kg bromocriptine administration was parallel to that of apomorphine. Consistent with the biochemical evidence that apomorphine's effects are mediated, to a lesser extent, by D1 activation, the apomorphine cue partially generalized to the selective D1 agonist SKF 38393. Furthermore, the apomorphine cue was not blocked by the selective D1 antagonist SCH 23390. Somewhat surprising was the partial generalization of the apomorphine cue to SCH 23390. However, this is not the first time that the administration of SCH 23390 has resulted in unexpected behavioral responses. Other novel findings include the lack of sex differences in acquisition training to the apomorphine cue and in the generalization tests to the selective agonists. The behavioral results are consistent with previous biochemical evidence that the effects of apomorphine are mediated by both D1 and D2 activation and is further behavioral support that apomorphine's effects are not the result of D2 activation alone, as previously hypothesized.

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