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Results for “Dopamine Agonists”

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At least 19 recordsLinked to original sources
PubMed1975

Inhibition by dopamine agonists of dopamine accumulation following gamma-hydroxybutyrate treatment.

The increase in the dopamine (DA) concentration of rat (whole) brain induced by gamma-hydroxybutyrate was inhibited by the reputed dopamine agonists apomorphine, apocodeine, 2-bromo-alpha-ergocryptine, piribedil, ergocornine and 5,6-dihydroxy-2-dimethylaminotetralin. The last three drugs raised DA levels in saline controls. Haloperidol, which decreased DA in controls slightly, prevented any agonist-induced rise in controls. However, haloperidol antagonized only apomorphine and piribedil in regard to the inhibition of the gamma-hydroxybutyrate induced rise in DA; this neuroleptic did not affect the inhibition by the other agonists. It is concluded that these data provide evidence for local receptor control of DA synthesis and that the DA agonists do not act through a common mechanism.

Animals↗
PubMed1978

The central effects of a novel dopamine agonist.

A new peripheral dopamine agonist which causes dopaminergic renal vasodilation, was tested for central dopaminergic activity. SK & F 38393 stimulated the dopamine-sensitive adenylate cyclase in homogenates of rat caudate, as a partial agonist, and caused contralateral rotation in rats with unilateral 6-OHDA lesions of substantia nigra. Rotation was shown to be due to a direct effect on supersensitive dopamine receptors. Stimulation of cAMP formation and rotation were blocked by dopamine antagonists. In contrast to other dopamine agonists, SK & F 38393 did not cause stereotypy, emesis or inhibition of prolactin release, nor did SK & F 38393 affect dopamine turnover. The results suggest that SK & F 38393 may selectively stimulate supersensitive central dopamine receptors in vivo or may activate only a certain subclass of dopamine receptors including the receptor in the renal vasculature and the adenylate cyclase coupled postsynaptic receptor in the caudate.

Adenylyl Cyclases↗
PubMed1979

Dopamine auto- and postsynaptic receptors: electrophysiological evidence for differential sensitivity to dopamine agonists.

The responses of dopamine cells in the substantia nigra to iontophoretically administered dopamine and intravenous apomorphine were compared to the responses of spontaneously active neurons in the caudate nucleus. Dopaminergic cells were six to ten times more sensitive to dopamine and intravenous apomorphine than 86 percent of the caudate cells tested. This differential sensitivity of dopamine auto- and postsynaptic receptors may explain the apparently paradoxical behavioral effects induced by small compared to large doses of some dopamine agonists and may provide a means of developing new types of drugs to antagonize dopaminergic influence in the central nervous system.

Action Potentials↗
PubMed1978

Effects of opiates on the discriminative stimulus properties of dopamine agonists.

Two groups of rats were trained to discriminate the dopamine agonists amphetamine (0.75 mg/kg) or apomorphine (0.38 mg/kg) from saline in a two-lever operant task. Various doses of morphine and pentazocine were tested for generalization to and interference with the discriminative stimulus complexes produced by the dopamine agonists. Low doses of morphine appeared to produce a stimulus complex which is similar to that produced by apomorphine, but which differs from the produced by amphetamine. Pentazocine showed no evidence of generalization to either the apomorphine or the amphetamine cue. Neither opiate interfered with discriminative stimuli produced by the dopamine agonists, although decreases in the number of animals responding occurred.

Amphetamine↗
PubMed1979

Effects of intranigral administration of dopamine agonists and antagonists and baclofen on concentrations of dopac and dopamine in the striatum and substantia nigra of the rat.

Systemic administration of haloperidol to rats failed to alter the concentration of dopamine but increased the concentration of 3,4-dihydroxy-phenylacetic acid (DOPAC), the major metabolite of dopamine, in both the striatum and substantia nigra. These haloperidol-induced changes in DOPAC were prevented by an intranigral microinjection of baclofen, a drug which reduces nigrostriatal dopaminergic neuronal activity. It has been proposed that nigrostriatal neurons are regulated, in part, by the activation of autoreceptors in substantia nigra. However, intranigral microinjections of high concentrations of several dopaminergic antagonists failed to mimic the biochemical effects resulting from systemic administration of these drugs; instead, they slightly increased the concentrations of both dopamine and DOPAC in the striatum and decreased dopamine in substantia nigra. Intranigral microinjections of the dopamine agonist, apomorphine, failed to alter the concentration of DOPAC in the striatum, but reduced both dopamine and DOPAC in the nigra. If DOPAC concentrations reflect nigrostriatal dopaminergic neuronal activity, the present results suggest that dopaminergic agonists and antagonists acting in substantia nigra do not exert a major influence on the activity of these neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Effect of dopamine agonist (Lergotrile mesylate) therapy on twenty-four hour secretion of prolactin in treated Parkinson's disease.

Plasma PRL was measured at 20-min intervals in six patients with Parkinson's disease under various treatment protocols. In addition, 24-h mean GH levels were measured. The results of these studies showed that two untreated patients with Parkinson's disease had normal 24-h mean PRL levels with the normal increase during sleep. During chronic treatment with L-dopa-carbidopa (Sinemet), the 24-h PRL level was 12.8 +/- 4.9 ng/ml (mean +/- SD) and there was persistence of augmented PRL secretion during sleep. The 24-h mean GH level ranged from 1.5-4.4 ng/ml, with a mean of 2.5 ng/ml. The addition of a dopamine agonist (Lergotrile mesylate) resulted in a significant (P less than 0.01) suppression of the 24-h mean PRL levels and abolition of the normal sleep augmentation after 2 weeks of therapy. This suppression was maintained in one patient who was restudied 4 months after the addition of dopamine agonist therapy to L-dopa-carbidopa. The 24-h mean GH levels did not change significantly after the addition of the dopamine agonist when compared to L-dopa-carbidopa alone. These results suggest a dichotomy between the PRL and GH responses to combined L-dopa-carbidopa and dopamine agonist therapy. In addition, the preservation of normal PRL regulation in the two untreated patients with Parkinson's disease suggests that dopaminergic neurons are not universally affected in this disorder.

Adult↗
PubMed1978

Clinical aspects of dopamine agonists and antagonists.

Dopamine and its specific receptors are widely distributed in man. Body regions where dopaminergic activity is of special pharmacologic interest include the basal ganglions, hypothalamus, chemoreceptor trigger zone, other less well defined areas in the central nervous system, and the renal and cardiovascular systems. The search for dopaminergic agents to modify these systems in disease states has depended heavily on in vitro and in vivo bioassays. These assays involving receptor binding, enzyme activation, smooth muscle and neuronal excitation, and modification of animal behavior have provided physicians with important therapeutic tools. Indeed, the introduction of levodopa for the treatment of Parkinson's disease and of the phenothiazines and related drugs for schizophrenia and psychosis has been a hallmark of neuropharmacologic research. However, the maximal benefits that these drugs may afford have not yet been realized due to an inadequate understanding of disease processes and a relative lack of specificity of drug action.

Adenylyl Cyclases↗
PubMed1977

Effects of dopamine agonists in tardive dyskinesia.

The authors used a combined behavioral and neuroendocrinological strategy to investigate the relevance of abnormalities in the brain dopaminergic systems to the pathophysiology of tardive dyskinesia by assessing the effects of apomorphine, a directly acting dopamine agonist, and d-amphetamine, an indirectly acting dopamine agonist, in patients with tardive dyskinesia. Administration of I.V. d-amphetamine increased dyskinetic movements in most patients with tardive dyskinesia, a finding consistent with the dopaminergic hypothesis. Contrary to predictions based on animal models, apomorphine did not increase dyskinetic movements in these patients but instead substantially reduced dyskinesia in some patients. Patients with tardive dyskinesia did not have a greater drop in serum prolactin or a greater rise in serum growth hormone after apomorphine than normal or chronic schizophrenic subjects without tardive dyskinesia.

Administration, Oral↗
PubMed1976

Alterations in the effects of dopamine agonists and antagonists on general activity in rats following chronic morphine treatment.

Results of two experiments revealed that morphine produced both time-and dose-dependent effects on the general activity of rats following a single acute administration, depression being observed 30 min after the injection and hyperactivity at 150 min. Tolerance to the depressive effects of morphine was observed within 7 days of chronic, once daily treatments, the depression being replaced by a hyperactivity that included a high degree of self-directed oral stereotyped behaviour. Dose-response analyses of the effects of d-amphetamine, an indirectly acting dopamine agonist, and apomorphine, a directly acting dopamine agonist, revealed a shift in the dose-response curves following chronic morphine treatment, indicating that the animals were supersensitive to these agents. Conversely, the dose-response curve for pimozide, a directly acting dopamine antagonist, was shifted in a direction indicating that the animals were subsensitive to this agent. The dose-response curve for haloperidol, another dopamine antagonist, was unchanged. These findings are consistent with the hypothesis that an increase in the number of dopamine receptors may develop during chronic treatment with morphine.

Animals↗
PubMed1978

Suppression of prolactin by dopamine agonists in schizophrenics and controls.

Prolactin levels were determined in plasma samples obtained before and after administration of apomorphine or L-dopa to otherwise unmedicated chronic schizophrenic patients or control subjects. Basal prolactin levels did not differ in these two groups. Suppression of prolactin levels after each dopamine agonist was highly significant. Suppression in schizophrenics was slightly less than in controls following apomorphine and slightly greater following L-dopa. The authors discuss the implications of these findings as well as the limitations of the prolactin regulatory system as an index of dopamine agonist sensitivity.

Adult↗
PubMed1977

The inhibitory effect of dopamine agonists on LH release in women.

Our demonstration of an inhibitory effect of dopamine on LH release prompted us to examine whether a similar action exists for dopamine agonists, such as L-dopa and 2-bromo-alpha-ergocryptine (CB-154). Following the administration of L-dopa (0.5 g, orally) to 6 normal women in the early follicular phase, a significant fall in mean LH levels after 1 h which lasted for 5 h was observed (P less than 0.00005). This was followed by a significant rebound above basal levels between the 7th and 10th h (P less than 0.00005). The expected fall in mean PRL levels which lasted for 4 h (P less than 0.00001) was followed by a significant rebound above basal levels after the 6th h (P less than 0.00001)). There was no significant change in mean FSH levels. Following the administration of CB-154 (2.5 mg. orally) to 6 women with hyperprolactinemic amenorrhea, there was also a significant fall in LH levels (P less than 0.00001) and in FSH levels (P less than 0.00001) from 5 h until the study ended at 10 h. The anticipated PRL suppression was also observed and persisted for the duration of the 10 h study. The demonstration of an inhibitory effect of L-dopa and CB-154 on LH release adds further support to the role of dopaminergic control of pituitary LH secretion.

Amenorrhea↗
PubMed1979

Dopaminergic supersensitivity: influence of dopamine agonists, cholinergics, anticholinergics, and drugs used for the treatment of tardive dyskinesia.

Single and repeated administration of neuroleptics induce supersensitivity to dopamine agonists like apomorphine and methylphenidate. The degree of this supersensitivity depends on the period of the preceding administration of the neuroleptic. In the development phase additional administration of apomorphine can reverse the hyperdopaminergic behaviour, whereas addition of cholinergic/anticholinergic treatment does not modify the enhanced receptor response. In the supersensitivity phase additional treatment with deanol does not modify the supersensitivity. Pheobarbital, diazepam, and muscimol increase and cis (Z)-flupenthixol decreases the supersensitivity. It is concluded that supersensitivity induced by neuroleptics is time-dependent and that it can be prevented by additional treatment with DA-agonists but not by cholinergic/anticholinergic treatment. In the supersensitivity phase, the syndrome is suppressed by dopamine antagonists but enhanced by GABA-agonists, benzodiazepine and phenobarbital.

Animals↗
PubMed1979

Dopamine agonists and cobalt-induced epilepsy in the rat.

1 Electrocorticogram (ECoG) recordings were made from conscious rats which had cortical implants of cobalt. The epileptiform spike activity was then assessed by means of an automated technique, based on peak angle measurements. 2 Apomorphine (0.5, 1.0 and 2.0 mg/kg i.p.) and lisuride (0.1, 0.25, 0.5 and 1.0 mg/kg i.p.) inhibited spike activity in established primary and secondary foci in a dose-dependent manner. Bromocryptine (10 and 20 mg/kg i.p.) and CF 25-397 (40 mg/kg i.p.) had a similar effect but only after a latent period of several hours. Chronic administration of bromocryptine (20 mg/kg i.p. daily) attenuated the normal development of the foci following implantation. 3 Pimozide (1 mg/kg i.p.) potentiated cortical epileptic activity in cobalt-implanted rats and blocked the antiepileptic effects induced by the dopamine agonists. 4 Intrastriatal administration of dopamine (25 micrograms) or apomorphine (60 micrograms) suppressed epileptiform spikes in the cortex. Destruction of striatal catecholamine terminals by 6-hydroxydopamine increased the spike activity. 5 It is concluded that the striatum may play an essential part in mediating the anti-epileptic effects of dopamine and its agonists in this model of epilepsy.

Animals↗
PubMed1979

[Dopa and dopamine agonists in depression (author's transl)].

Following a summary of the functional organisation of the ascending dopamine systems, the pharmacology of the dopamine synaptic receptors is considered. The stress is placed upon the differences induced by dopamine agonists during short-term and long-term treatment. In this connection, recent ideas on the heterogeneous nature of the dopamine receptors, on their specificity and on their functional role will be discussed. The dopaminergic action of certain antidepressants will be studied by analysing the different types of activity: presynaptic release, direct pre- or post-synaptic agonism. The role of dopaminergic transmission in depression of mood is considered finally on the basis of clinico-biochemical correlations. Finally, dopaminergic activity is linked with the other possible changes in cerebral monoamines by drafting a table of the interactions between the neurotransmitters.

Animals↗