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At least 469 records · Page 26Linked to original sources
PubMed1985

A comparison between dopamine-stimulated adenylate cyclase and 3H-SCH 23390 binding in rat striatum.

Methods for measuring 3H-SCH 23390 binding and dopamine (DA) stimulated adenylate cyclase (AC) were established in identical tissue preparations and under similar experimental conditions. Pharmacological characterization revealed that both assays involved interaction with the D1 receptor or closely associated sites. In order to investigate whether the binding sites for 3H-SCH 23390 and DA in fact are identical, the antagonistic effects of a variety of pharmacologically active compounds were examined. Surprisingly, the Ki-values obtained from Schild-plot analysis of the antagonism of DA-stimulated AC, were 80-240 times higher than the Ki-values obtained from competition curves of 3H-SCH 23390 binding. Since both assays were performed under identical conditions, the differences in Ki-values indicate the possibility of different binding sites for DA and 3H-SCH 23390 or, that DA and 3H-SCH 23390 label different states of the same receptor.

Adenylyl Cyclases↗
PubMed1982

Interaction of opiates with dopamine receptors: receptor binding and behavioral assays.

We examined the hypothesis that opiates act as dopamine (DA) receptor-blocking agents thereby inducing a compensatory increase in DA receptor density during chronic administration, and that increased receptor density could account for the behavioral hypersensitivity to DA agonists seen after treatment with opiates. Morphine and methadone did not inhibit the specific binding of 3H-spiroperidol to DA receptors in vitro, nor did they decrease affinity or apparent receptor density in the striatum when administered acutely in vivo in behaviorally effective doses. In contrast, neuroleptics had the expected inhibitory effect in both these experiments. Stereotypy and locomotion in response to apomorphine were measured before and after a 3-week treatment with saline or methadone. About half the methadone-treated rats showed significant increases over predrug baselines in stereotypy or locomotion, as did a few saline-treated animals. However, in those animals showing enhanced stereotypy or locomotion, DA receptor density was not elevated in striatum or mesolimbic areas respectively. These results indicate that opiates do not act as antagonists at DA receptor sites, and that changes in DA receptor density cannot account for opiate-induced behavioral hypersensitivity.

Animals↗
PubMed1982

Multiple postsynaptic dopamine receptors and behavioral manifestation.

Previously we demonstrated the existence of non- and positive-cooperative dopamine receptors in rat striatum in [3H] apomorphine binding experiments. Non-cooperative sites were sensitive to the inhibition of sulpiride while cooperative sites were not. In the present study results dealing with the involvement of those two types of postsynaptic dopamine receptors in different behavior manifestations is shown employing lisuride hydrogen maleate (LHM). LHM elicited contralateral turnings in 6-hydroxydopamine lesioned rats unilaterally in the striatum whereas it caused ipsilateral turnings in kainic acid lesioned rats as was observed following the administration of apomorphine. Furthermore, the effect of LHM on rotating behavior was abolished by the pretreatment with sulpiride. On the other hand, LHM inhibited apomorphine induced stereotyped behavior whereas the sulpiride failed to block it. These results suggested the dual action of LHM on multiple postsynaptic dopamine receptors. The results also indicated that non-cooperative postsynaptic dopamine receptors are involved in rotating behavior while cooperative receptors participate in the elicitation of stereotypy.

Animals↗
PubMed1985

Binding of 3H-spiperone to human lymphocytes: a biological marker in schizophrenia?

The specific binding of the dopamine antagonist 3H-spiperone to lymphocytes from a healthy control group (n = 40), a group of acute, unmedicated schizophrenic patients (n = 27), and a psychiatric control group (n = 16) was investigated. There were no differences in binding parameters between the healthy controls (Bmax 2.6 +/- 0.7 fmoles/10(6) cells; Kd 0.17 +/- 0.07 nM) and the psychiatric control group. Binding capacity of 3H-spiperone was significantly increased in lymphocytes from the schizophrenic patients (Bmax 14.4 +/- 9.3 fmoles/10(6) cells). Moreover, a slight decrease in affinity was observed (Kd 0.44 +/- 0.21 nM). Because the increase in binding appeared only in schizophrenic patients, this peripheral model could prove valuable as a diagnostic criterion.

Acute Disease↗
PubMed1984

Differential ontogenesis of D1 and D2 dopaminergic receptors in the chick embryo retina.

The differentiation of D1 and D2 dopamine receptors was investigated during the ontogenesis of the chick embryo retina. Our results reveal an interesting complexity in dopaminergic differentiation, with one major receptor system developing before synapses and another one developing after. The dopamine-dependent increase of chick retina cAMP level differentiates early during retina ontogeny. By the embryonic day 10-11 10(-4) M dopamine and ADTN elicit a 13-fold increase in cAMP content of the retina. However, [3H]spiperone (D2 ligand) binds very little to crude membrane preparation of retinas from embryos in the same developmental stage (12-13 fmol/mg protein). High specific binding of [3H]spiperone is only detected after the embryonic day 17-18, attaining 80 to 100 fmol of specific spiperone binding sites in the retinas from post-hatched animals. Apomorphine also promotes the accumulation of cAMP of retinas from early embryonic stages. However, it is only 20-30% as effective as ADTN or dopamine. In addition, while the dopamine responsiveness of the tissue decreases sharply during its ontogeny, the apomorphine effect remains practically constant throughout this period. Both dopamine and apomorphine are equally effective in eliciting cAMP accumulation of retinas from post-hatched animals. Moreover, apomorphine is a potent inhibitor of dopamine-induced cAMP level of the embryonic tissue. The results presented here indicate that D1 and D2 receptors differentiate independently from each other, and that apomorphine elevates retina cAMP levels via a subclass of D1 receptors that does not desensitize significantly during retina development.

Animals↗
PubMed1984

Spiroperidol binding sites on mouse lymphoid cells. Effects of ascorbic acid and psychotropic drugs.

Since highly differentiated cells of mammalian immune systems reportedly have binding sites for a variety of neurohumoral agents, we investigated parameters related to possible existence of dopamine receptors on murine lymphoid cells. Using a dopamine antagonist, [3H]spiroperidol, we found evidence for displaceable binding on mouse spleen cells. Total and displaceable (10 microM haloperidol) binding of spiroperidol was markedly enhanced by the absence of ascorbic acid in the incubation medium. Displaceable binding of a dopamine receptor agonist [( 3H]ADTN) could not be found on lymphoid cells either in the presence or absence of ascorbic acid. In the absence of ascorbate, displaceable spiroperidol binding to mouse spleen cells revealed partially saturable, but complex, kinetics and we calculated positive cooperativity at low ligand concentrations.

Animals↗
PubMed1984

The effects of denervation and chronic haloperidol treatment on neostriatal dopamine receptor density are not additive in the rat.

The effects of combined denervation and chronic haloperidol treatment on neostriatal D-2 receptor density were examined, and a lack of additivity was found. In the first experiment, haloperidol treatment for 14 days initiated on day 4 after the unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) abolished the lesion-induced asymmetry of [3H]spiroperidol binding by elevating the density of sites in the intact striatum. These results were replicated in the second experiment, in which the drug treatment was begun 4-5 weeks after 6-OHDA. In both experiments the apomorphine-induced rotation did not differ significantly between lesioned rats treated with haloperidol or its vehicle.

Animals↗
PubMed1984

Quantitative autoradiography of [3H]sulpiride binding sites in rat brain.

A technique has been developed to investigate [3H]sulpiride binding in rat brain sections using quantitative autoradiography and tritium-sensitive film. Binding was saturable and reversible with very low nonspecific binding. [3H]Sulpiride bound to an apparent single population of sites in striatum with a Kd of 3.2 nM and Bmax of 447 fmol/mg protein. Binding sites were localized in the lamina glomerulosa of the olfactory bulb, nucleus accumbens, olfactory tubercle, striatum and substantia nigra.

Animals↗
PubMed1985

In vitro demonstration of dopamine uptake by neostriatal serotonergic neurons of the rat.

Dopamine (DA) has been suggested as the penultimate agent in the neurotoxic effects of methamphetamine on serotonergic neurons. DA increases the efflux of tritium from rat neostriatal slices preloaded with [3H]serotonin in a concentration-dependent manner. This serotonin (5-HT) release is inhibited by the same selective uptake blockers previously shown to protect serotonergic neurons from the neurotoxic effects of methamphetamine in vivo. The results indicate that the 5-HT uptake carrier transports DA into the serotonergic neuron by a heteroexchange process with 5-HT. This further suggests that the excessive DA release induced by methamphetamine in vivo could lead to the uptake of DA into serotonergic neurons.

Animals↗
PubMed1985

Inhibition of inositol phospholipid breakdown by D2 dopamine receptors in dissociated bovine anterior pituitary cells.

Inositol phospholipids have been labelled with [3H]inositol in a lactotroph-enriched preparation of dissociated bovine anterior pituitary cells. Stimulation of cells with thyrotropin-releasing hormone receptor agonists leads to accumulation of [3H]inositol phosphates, and this effect may be inhibited by dopamine (DA) agonists. The DA agonist effect may be prevented by D2 DA receptor selective antagonists. Thus the D2 receptors on these cells are linked to inhibition of inositol phospholipid metabolism, and this provides a functional assay for the receptor.

Animals↗
PubMed1990

Regulation and molecular characterization of dopamine D2 receptors in a prolactin-secreting 7315a anterior pituitary tumor.

The regulation and molecular properties of the dopamine (DA) D2 receptors were compared in the prolactin-secreting 7315a anterior pituitary tumor with those in the striatum of rats. Chronic treatment with haloperidol increases the maximal binding for [3H]spiroperidol in tumor and striatum, but the percent increase is much higher in tumor than in striatum. Photoaffinity labelling of DA D2 receptors with N-(p-azido-m-[125I]iodophenethyl)spiperone ([125I]N3-NAPS) yielded a major specifically labeled peptide with the Mr of 32-34 kDa in tumor, and two specifically labeled peptides with Mr of 32-34 and 92-94 kDa in striatum. The analysis of DA D2 receptor mRNA shows that the size is similar in tumor and striatum. The DA D2 receptor mRNA in tumor is very low and chronic treatment with haloperidol produces a considerable increase of the specific mRNA. It is postulated that the reported defect in regulation of prolactin release by DA agonists might be due to posttranslational changes in the tumor DA D2 receptor.

Animals↗
PubMed2004

Investigation of the mechanism of agonist and inverse agonist action at D2 dopamine receptors.

This study investigated, for the D2 dopamine receptor, the relation between the ability of agonists and inverse agonists to stabilise different states of the receptor and their relative efficacies. Ki values for agonists were determined in competition versus the binding of the antagonist [3H]spiperone. Competition data were fitted best by a two-binding site model (with the exception of bromocriptine, for which a one-binding site model provided the best fit) and agonist affinities for the higher (Kh) (G protein-coupled) and lower affinity (Kl) (G protein-uncoupled) sites determined. Ki values for agonists were also determined in competition versus the binding of the agonist [3H]N-propylnorapomorphine (NPA) to provide a second estimate of Kh. Maximal agonist effects (Emax) and their potencies (EC50) were determined from concentration-response curves for agonist stimulation of guanosine-5'-O-(3-[32S]thiotriphosphate) ([35S]GTPgammaS) binding. The ability of agonists to stabilise the G protein-coupled state of the receptor (Kl/Kh determined from ligand-binding assays) did not correlate with either of two measures of relative efficacy (relative Emax, Kl/EC50) of agonists determined in [35S]GTPgammaS-binding assays, when the data for all of the compounds tested were analysed. For a subset of compounds, however, there was a relation between Kl/Kh and Emax. Competition-binding data versus [3H]spiperone and [3H]NPA for a range of inverse agonists were fitted best by a one-binding site model. Ki values for the inverse agonists tested were slightly lower in competition versus [3H]NPA compared to [3H]spiperone. These data do not provide support for the idea that inverse agonists act by binding preferentially to the ground state of the receptor.

Animals↗