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PubMed1981

Actions of dopamine and apomorphine on the vasoconstrictor responses of perfused mesenteric arteries of mouse, rat and rabbit.

Dopamine (10(-7)--10(-6) M) and apomorphine (5 x 10(-7)--5 x 10(-6) M) inhibited the vasoconstrictor responses of the perfused mesenteric artery preparations of rat, rabbit and mouse to adrenergic nerve stimulation but did not affect responses to added noradrenaline. The inhibitory effects of both dopamine and apomorphine were prevented by haloperidol (3 x 10(-7) M) but not by yohimbine (3 x 10(-8) M) in rat and rabbit mesenteric artery preparations. In contrast, yohimbine (3 x 10(-8) M), but not haloperidol, antagonized the inhibitory effect of dopamine and apomorphine in mouse mesenteric artery preparations. In higher concentrations, dopamine (10(-6)--10(-4) M) produced a direct vascoconstrictor effect, which involved post-junctional alpha-adrenoceptors in all three species. However, in preparations contracted with 10(-7) M 5-hydroxytryptamine and in the presence of phentolamine (3 x 10(-7) M) and propranolol (10(-6) M), dopamine (10(-6)--10(-4) M) produced a direct relaxant effect in rabbit mesenteric artery preparations but not in those of rat and mouse. It is suggested that inhibition of neurogenic vasoconstrictor responses, by dopamine and apomorphine, may be mediated through a specific prejunctional inhibitory dopamine receptor in the mesenteric artery of rat and rabbit whereas in the mouse they involve activation of alpha-adrenoceptors.

Animals↗
PubMed1984

Differential effects of 5-hydroxytryptaminergic antagonists upon apomorphine- and lergotrile-induced hypothermia and stereotyped behaviour in rats.

The dopaminergic stimulants apomorphine and lergotrile both evoked hypothermia and stereotyped behaviour in rats. These drug effects were sensitive to antagonism by haloperidol, a dopaminergic receptor blocker. In rats pretreated with 5-hydroxytryptaminergic receptor blockers, cinanserin reduced apomorphine-induced hypothermia but cyproheptadine did not. Both cinanserin and cyproheptadine significantly potentiated lergotrile-induced hypothermia. Similarly, the stereotypic effects of apomorphine were partly reduced by cyproheptadine, although higher doses of cyproheptadine did potentiate lergotrile-induced stereotyped behaviour. These findings of different influences of 5-HT antagonists upon the effects of apomorphine and lergotrile indicate that these two dopaminergic stimulants may not work in identical manner to produce outwardly similar drug effects.

5-Hydroxytryptophan↗
PubMed1988

Chronic antidepressant treatment increases the apomorphine-induced elevation of plasma corticosterone in rats.

Plasma corticosterone concentrations in response to subcutaneous administration of apomorphine (25 and 200 micrograms kg-1) have been assessed in rats treated acutely (2 days) or repeatedly (15 days) with saline, clomipramine, electroshock and clomipramine + electroshock. Chronic, but not acute, antidepressant treatment decreased the corticosterone level which remained unchanged in control and in rats acutely treated with apomorphine. Chronic antidepressant treatment significantly increased the corticosterone response to apomorphine. Neuroendocrine evidence is provided for an increased responsiveness of dopamine receptors which are thought to mediate the apomorphine effect on corticosterone secretion following chronic antidepressant treatment.

Animals↗
PubMed1990

Desipramine and nortriptyline antagonize apomorphine and reserpine hypothermia by a different mechanism.

The reversal of hypothermia, induced by reserpine or by a high (16 mg) dose of apomorphine, in male Swiss mice, does not seem to utilize a common mechanism. Desipramine (20 mg kg-1 i.p., 60 min) or nortriptyline (8 mg kg-1 i.p., 60 min) increased temperature in both reserpine (2.5 mg kg-1 s.c., 18-19 h) and apomorphine (16 mg kg-1 s.c., 30 min) treated mice. In apomorphine-treated animals the effect of both drugs was reversed by the mixed dopaminergic D1- D2-antagonist haloperidol (1 mg kg-1 i.p., 90 min), the D1-receptor blocking drug SCH 23390 (0.05 mg kg-1 s.c., 30 min), the alpha 1-adrenoceptor blocking drugs prazosin (3 mg kg-1 s.c., 90 min) and phenoxybenzamine (20 mg kg-1 i.p., 65 min), the beta-adrenoceptor blocking drug (+/-)-propranolol (10 mg kg-1 i.p., 120 min), and the opioid antagonist naloxone (2 mg kg-1 i.p., 15 min). In contrast the selective D2-antagonist (+/-)-sulpiride (100 mg kg-1 i.p., 90 min), and the alpha 2-antagonist yohimbine (2 mg kg-1 i.p., 75 min), failed to effect the reversal of apomorphine hypothermia brought about by desipramine or nortriptyline. Their temperature effects in reserpinized mice were not modified by any of the antagonists tested.

Animals↗
PubMed1974

Apomorphine: modification of its hyperthermic effect in rabbits by p-chlorophenylalanine.

The hyperthermic response of rabbits to apomorphine, a dopaminergic agonist, is abolished by prior treatment with p-chlorophenylalanine. If such 5-hydroxytryptamine (5-HT)-depleted animals are administered a peripherally acting decarboxylase inhibitor plus 5-hydroxytryptophan, central stores of 5-HT are regenerated and the hyperthermic response to apomorphine is restored in part. The effects of apomorphine in rabbits with elevated concentrations of 5-HT are not different from those in control animals. The behavioral effects of apomnorphine appear to be constant in all groups of animals tested. It is suggested that the hyperthermic effects of apomorphine in rabbits require the presence of 5-HT.

Animals↗
PubMed1975

Apomorphine and psychopathology.

Forty men, mainly alcoholics, were administered either the dopamine receptor agonist, apomorphine HCl (1 mg), or distilled water subcutaneously three times a day for 14 days in a double blind study. None of the subjects developed an endogenous depression or schizophrenic symptoms. Scores on the Hamilton Rating Scale, Zung Self Rating Scale, and Brief Psychiatric Rating Scale showed improvement with both apomorphine and placebo. There were no significant differences between the two treatments on these rating scales. A significant incidence of spontaneous penile erections occurred after apomorphine treatment compared with placebo. Both treatments eliminated subjective craving for alcohol. Acute administration of apomorphine had no effect on psychomotor retardation or depressed mood in two patients with endogenous depression.

Alcoholism↗
PubMed1994

Apomorphine induced cognitive changes in Parkinson's disease.

Auditory event related potentials (ERPs) and visual evoked potentials (VEPs) were recorded from eight patients with Parkinson's disease, before and after a single dose of apomorphine. To assess the treatment effects, the patients' motor state, Benton visual retention test (BVRT), and digit span tests were also examined. After apomorphine, although motor performance improved, the ERP latencies were delayed and the N2-P3 ERP amplitude was significantly diminished by comparison with pretreatment values. These data suggest that apomorphine induces, besides its motor effects in patients with Parkinson's disease, a slowing down of cognitive processing. Preferential stimulation of dopamine autoreceptors in mesocortical and mesolimbic systems may represent a neural mechanism for these effects. Also, the posttreatment BVRT rotation errors significantly increased, suggesting an apomorphine induced impairment of visuospatial perception.

Apomorphine↗
PubMed1998

Continuous subcutaneous waking day apomorphine in the long term treatment of levodopa induced interdose dyskinesias in Parkinson's disease.

OBJECTIVES: To determine whether continuous waking day dopaminergic stimulation with the dopamine agonist apomorphine can reduce levodopa induced dyskinesias in Parkinson's disease METHODS: 19 patients with severe unpredictable refractory motor fluctuations and functionally disabling levodopa induced dyskinesias were treated with continuous subcutaneous apomorphine monotherapy for a minimum duration of 2.7 years RESULTS: A mean 65% reduction in dyskinetic severity and a mean 85% reduction in frequency and duration occurred. On discontinuing levodopa a concomitant reduction in off period time was also seen (35% of waking day "off" reduced to 10%) CONCLUSION: Continuous waking day dopaminergic stimulation with apomorphine reset the threshold for dyskinesias and led to a pronounced reduction in their frequency. Apomorphine should be considered as a less invasive alternative to pallidotomy or deep cerebral stimulation in controlling levodopa induced interdose dose dyskinesias.

Aged↗
PubMed1979

Effects of apomorphine on thermoregulatory responses of rats to different ambient temperatures.

Either systemic or central administration of apomorphine produced dose-related decreases in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C in rats. At Ta = 8 degrees C, the hypothermia was brought about by a decrease in metabolic rate (M). At Ta = 22 degrees C, the hypothermia was due to an increase in mean skin temperature, an increase in respiratory evaporative heat loss (Eres) and a decrease in M. This increased mean skin temperature was due to increased tail and foot skin temperatures. However, at Ta = 29 degrees C, apomorphine produced increased rectal temperatures due to increased M and decreased Eres. Moreover, the apomorphine-induced hypothermia or hyperthermia was antagonized by either haloperidol or 6-hydroxydopamine, but not by 5,6-dihydroxytryptamine. The data indicate that apomorphine acts on dopamine neurons within brain, with both pre- and post-synaptic sites of action, to influence body temperature.

5,6-Dihydroxytryptamine↗
PubMed1980

Effects of apomorphine and pimozide on temperature regulation during exercise in the rat.

The purpose of this study was to determine the effects of a specific dopamine receptor agonist (apomorphine) and antagonist (pimozide) on thermoregulation when the heat loss pathway was activated by the stress of exercise. Apomorphine or its control vehicle (0.9% wt/vol saline) was injected systemically (0.5, 1.0, 1.5 mg/kg ip) or within the preoptic-anterior hypothalamus (5, 10, 20 micrograms) immediately before the start of treadmill exercise at 21.5 m/min. Colonic, tailskin, and ambient temperatures were recorded each minute. Oxygen consumption was calculated from on-line measurements of percent O2 and CO2. Pimozide injected systemically (0.5 mg/kg ip) had no effect on resting colonic temperature, but caused a significant (P less than 0.05) hyperthermia during treadmill exercise compared to saline controls. Central and systemic injections of apomorphine caused a dose-dependent hypothermia that was blocked by pretreatment with pimozide. Oxygen uptake values during exercise following the central injection of apomorphine were virtually identical to those following the injection of saline, but colonic temperature was significantly (P less than 0.05) lower than saline controls, indicating that the hypothermia observed was not due to a reduction in metabolic rate. These data indicate that dopamine receptors in the preoptic-anterior hypothalamus of the rat participate in the mediation of heat dissipation when the animal is challenged with a heat stress.

Animals↗
PubMed2004

Nitric oxide agents and apomorphine-induced rat behaviors.

BACKGROUND: Nitric oxide (NO) may alter dopamine release in the brain. Activation of D2-dopamine receptors may suppress NO synthase, and inhibition of NO synthase prevents behaviors induced by psychostimulants. We have investigated the modulatory actions of the precursor of NO synthesis (L-arginine) and the broad-spectrum NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on apomorphine-induced behaviors in the rat. METHODS: Apomorphine was injected subcutaneously, and behaviors induced by the drug were examined in the presence or absence of intracerebroventricular administration of L-arginine and L-NAME. RESULTS: Our data indicate that L-arginine or L-NAME treatment decreased licking and yawning, but not penile erection induced by apomorphine. CONCLUSION: Apomorphine-induced behaviors may be modulated by NO levels.

Animals↗
PubMed1975

Apomorphine-induced aggression: an evaluation of possible sensitizing factors in the rat.

The effects of prior experience with fighting and prior experience with both apomorphine and fighting were evaluated as possible sensitizing factors in rat intraspecific aggression induced by apomorphine. Results revealed that prior experience with the drug alone, or with fighting alone, had no effect on apomorphine-induced aggression. However, animals that had previously fought under the influence of apomorphine showed even higher levels of aggression suggesting that repeated experience with both the drug and fighting induces a type of sensitization.

Aggression↗
PubMed1984

Clinical effects of apomorphine in schizophrenia.

There have been reports that low doses of the dopamine-agonist apomorphine, which may inhibit dopamine neurotransmission, are of therapeutic benefit in schizophrenia. We conducted a placebo-controlled study of acute and chronic schizophrenics in which videotaped interviews were blindly rated. No specific therapeutic effect was demonstrated for apomorphine other than a reduction in anxiety in acute schizophrenics. Furthermore, there was no difference in the frequency of side-effects of apomorphine between schizophrenic patients and controls, and no specific effect of apomorphine on blink-rates. These findings emphasize the importance of placebo-controlled studies in schizophrenia research.

Acute Disease↗
PubMed1984

Hormonal effects of apomorphine in schizophrenia.

The hormonal effects of apomorphine, a direct-acting dopamine receptor agonist, in schizophrenic patients are of interest in view of the therapeutic efficacy of dopamine receptor antagonists. In this study, apomorphine (0.75 mg s.c.) and placebo were administered to unmedicated acute and chronic schizophrenics and controls. Apomorphine-induced prolactin suppression did not discriminate between the groups. However, an inverse relationship between basal prolactin levels and the severity of positive symptoms was detected in the patients with acute schizophrenia, consistent with a role for dopamine in the genesis of these symptoms. Growth hormone increments after apomorphine administration were blunted in the chronic schizophrenic patients, particularly those with 'negative' symptoms. It is argued that this blunting is not due to previous neuroleptic therapy and may represent evidence of structural change in the hypothalamus in this group of patients.

Acute Disease↗
PubMed1988

Blunted response of growth hormone to clonidine and apomorphine in endogenous depression.

We measured the growth hormone (GH) response to clonidine (an alpha-2-adrenergic agonist) and to apomorphine (a dopaminergic agonist) in 15 major endogenous and 15 minor depressive in-patients matched for gender and age. Results showed a significantly smaller GH response in the major depressives to both clonidine (P less than 0.01) and apomorphine (P less than 0.001). No significant difference existed between the two groups with regard to changes in blood pressure and pulse rate during either test. While major depressives showed a trend toward smaller sedative side-effects than minor depressives after clonidine, they showed significantly smaller sedative and gastro-intestinal side-effects after apomorphine. No significant correlation was present either in the major depressive or in the minor depressive group between the GH responses following clonidine and apomorphine challenges. These results support the hypothesis of both noradrenergic and dopaminergic neurotransmitter disturbances in major depression, with individual variability with regard to those biochemical anomalies.

Adult↗
PubMed1980

Transient abolition of generalized photosensitive epileptic discharge in humans by apomorphine, a dopamine-receptor agonist.

Apomorphine, an agonist of dopamine receptors, blocks or significantly reduces photically induced seizures in the baboon (Papio papio). We therefore studied the effect of subcutaneously administered apomorphine in 11 patients with generalized photosensitive epilepsy. Visual evoked potentials were not altered by apomorphine, but in nine patients apomorphine transiently blocked the epileptic photosensitivity for an average of 45 minutes. Therefore, dopaminergic mechanisms play a role in the pathophysiology of human generalized photosensitive epilepsy.

Adolescent↗
PubMed1992

Time interval between repeated injections conditions the duration of motor improvement to apomorphine in Parkinson's disease.

Behavioral hyposensitivity to repeated apomorphine administration occurs in fluctuating parkinsonian patients. To determine to what extent the interval between doses influences the response, we administered equal paired apomorphine injections to 10 fluctuating parkinsonian patients. Subjects received two apomorphine injections at 2-hour and at 4-hour intervals on different days after a 10- to 12-hour overnight period without levodopa. Following apomorphine doses at 2-hour intervals, the duration of response was reduced by 40% (61 versus 42 minutes, p less than 0.001) but was of equal duration when the doses were given at 4-hour intervals. These findings indicate that the interval between doses is a critical determinant of motor response. We postulate a time-dependent period of partial hyposensitivity to pulsatile DA stimulation.

Adult↗
PubMed1993

Parkinson's disease and somatosensory evoked potentials: apomorphine-induced transient potentiation of frontal components.

We recorded somatosensory evoked potentials (SEPs) to median nerve stimulation from parietal and frontal districts in 32 patients with Parkinson's disease by evaluating latency/amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and 10, 20, 30, and 60 minutes after subcutaneous administration of apomorphine chloride. The frontal complex N30-P40 was smaller than normal in 17 patients in baseline recordings. Following apomorphine, the parietal responses did not significantly vary in amplitude, but the frontal complex showed a remarkable amplitude potentiation in 22 of 32 patients (68.7%, p < 0.001), 19 of whom were also improving clinically. Amplitude potentiation was evident 10 minutes after apomorphine and faded away nearly in parallel with the end of its clinical efficacy. There were no SEP changes in three healthy controls after apomorphine.

Adult↗