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At least 199 records · Page 11Linked to original sources
PubMed1993

3H-spiperone binding to lymphocytes fails in the differential diagnosis of de novo Parkinson syndromes.

In order to investigate the diagnostic value of 3H-spiperone binding capacity to lymphocytes in the differential diagnosis of de novo Parkinson's disease (idiopathic Parkinson syndrome, PD), we performed a double blind prospective study of spiperone binding capacity of 123 patients and 23 healthy control persons, belonging to different diagnostic groups (PD, Parkinsonian syndrome due to vascular lesions, multiple system atrophy [MSA], essential tremor). Diagnoses were based on medical history, clinical examination, CT or MRI scan, acute response to dopamimetic drugs, one year follow up, and long term response to L-DOPA treatment. Spiperone binding was assayed using ten different concentrations (0.03-3 nmol) in absence or presence of 1 mumol (+)-butaclamol to determine nonspecific binding. There was no significant difference in spiperone binding between patients with PD not treated with L-DOPA, and patients with other basal ganglia disorders including parkinsonian syndrome due to vascular lesions, multiple system atrophy, or progressive supranuclear palsy, and age matched controls. Binding was significantly higher in parkinsonian patients with PD treated with L-DOPA and patients with essential tremor. It is concluded that at present 3H-spiperone binding gives no further information in the differential diagnosis of de novo Parkinson's disease.

Adult↗
PubMed1992

Binding of [3H]SCH23390 to a non-dopaminergic site in bovine kidney.

Binding of the D1 dopamine receptor antagonist [3H]SCH23390 to bovine renal cortical membranes has been studied. Specific binding of [3H]SCH23390 was saturable and reversible and stereoisomers of SCH23390 competed stereoselectively. In contrast, competition with the isomers of butaclamol was not stereoselective and dopamine failed to compete for the [3H]SCH23390 binding site. The site is therefore not a D1 dopamine receptor. Competition studies with a very wide range of compounds failed to define the nature of the [3H]SCH23390 binding sites in renal cortex whereas in parallel studies the characteristics of [3H]SCH23390 binding in caudate nucleus were entirely consistent with those of D1 dopamine receptors. The nature of [3H]SCH23390 binding in preparations of tubular and glomerular membranes was found to be virtually identical to those of crude renal cortical membranes indicating lack of compartmentation of these sites. Autoradiographic studies of [3H]SCH23390 binding in bovine kidney showed significantly higher levels of binding sites in renal cortex compared with renal medulla and this was confirmed by direct ligand binding studies.

Animals↗
PubMed1980

Reduced dopaminergic binding during aging in the rodent striatum.

[3H]Spiroperidol and [3H]ADTN ( 2-amino-l,7-dihydroxy-1,2,3,4-tetra hydronaphthalene) binding were used to assay for dopamine receptors in aged C57BL/6J mouse striatal membranes. [3H]spiroperidol binding declined linearly with age starting at 3 months. By 28 months, spiroperidol binding was only about 50% of the 3 month value. Dissociation constants dissociation rates and binding inhibition by (+)-butaclamol (antagonist) and apomorphine (agonist) were similar, suggesting that the age-related loss of spiroperidol binding was due to a loss in receptor number and not an alteration in binding affinity. [3H]ADTN binding also declined with age, but the losses tended to be about twice as large as those seen for spiroperidol. Consideration of possible mechanisms of receptor loss with age indicate that nigrostriatal denervation effects cannot explain all aging changes in striatal dopaminergic functions. The loss of receptors with age may derive from a loss of striatal neurones on which residue a population of dopaminergic binding sites.

Aging↗
PubMed1987

Acute thioridazine stimulates mesolimbic but not nigrostriatal dopamine release: demonstration by in vivo electrochemistry.

In vivo electrochemical techniques were employed to demonstrate that haloperidol and (+)-butaclamol increased the release of dopamine (DA) in the striatum and nucleus accumbens, whereas thioridazine stimulated DA release only in the accumbens. The stimulatory effect of thioridazine was reversed by gamma-butyrolactone. Given that gamma-butyrolactone inhibits DA neuronal activity, these data indicate that the regional selectivity of thioridazine on DA release is due to its ability to preferentially stimulate DA cell firing in the ventral tegmental (A10) area and suggest that its antipsychotic properties depend on its actions in the mesolimbic DA system.

4-Butyrolactone↗
PubMed1988

Long-term enhancement (LTE) of postsynaptic potentials following neural conditioning, in mammalian sympathetic ganglia.

Orthodromic, preganglionic conditioning stimulation can consistently induce long-term enhancement (LTE) (greater than 3 h) of the muscarinically mediated slow excitatory postsynaptic potential and the slow inhibitory postsynaptic potential. This was shown for superior cervical ganglia of rabbit and rat. Effective conditioning stimuli are in a physiologically observed range (3/s for 7 min, 5/s for 4 min, 10/s for 2 min, 20/s for 1 min). LTE was producible both homosynaptically and heterosynaptically. LTE can thus be associative, with conditioning synaptic input in one line inducing long-term changes in postsynaptic responses to another (heterosynaptic) input. The dopamine antagonist butaclamol depressed LTE, particularly that following the initial postconditioning period of 30 min. Adrenergic antagonists had no effect. This pharmacological evidence, coupled with the heterosynaptic induction of LTE, supports the view that neurally induced LTE may be at least partly mediated by endogenous dopamine. Another non-cholinergic but non-adrenergic transmitter (possibly a peptide) might contribute to the LTE seen in the initial 30 min postconditioning. The present, orthodromically induced LTE is clearly different from the long-term potentiation widely studied in hippocampus, etc., in the modes of induction and synaptic mediation.

Animals↗
PubMed1984

The binding of [3H]N-(chloroethyl)-norapomorphine to rat striatal membranes.

N-(chloroethyl)-norapomorphine (NCA) irreversibly inhibits striatal dopamine function, the binding of dopamine agonist ligands and dopamine-stimulated adenylate cyclase. A selective interaction of [3H]NCA with dopamine receptor sites would be of use in the characterisation and isolation of brain dopamine receptors. In this study the binding of [3H]NCA to homogenates of rat striatum was investigated. Binding of [3H]NCA to striatal preparations was saturable and irreversible and prevented with high affinity by dopamine agonist drugs with a catechol moiety. However, binding was not prevented in a stereoselective manner by the isomers of butaclamol, flupenthixol or sultopride. Nor was [3H]NCA binding specific to brain areas containing dopamine receptors. We conclude that [3H]NCA binding is not selective for dopamine receptors, although NCA inhibited both [3H]N,n-propylnorapomorphine (NPA) and [3H]spiperone binding in a non-competitive manner.

Amisulpride↗
PubMed1985

The effect of dopamine upon oxidative metabolism of brown fat adipocytes.

The effect of dopamine upon the oxygen consumption (QO2) of brown fat adipocytes was measured by polarography. The results showed a marked stimulation of QO2 by dopamine, similar to that induced by noradrenaline. The dopamine response could be blocked by haloperidol, butaclamol, propranolol and by high concentrations of tolazoline. These results suggest a role for dopamine in energy release from brown fat.

Adipose Tissue, Brown↗
PubMed1990

The effects of ions and hypothalamic factors on the in vitro activity of rainbow trout prolactin cells.

The influence of various ions and of dopamine and somatostatin on the in vitro activity of rainbow trout prolactin (PRL) cells was investigated. There was a positive correlation between medium Ca2+ concentration and both PRL synthesis and release up to 1.8 mM Ca2+, above which no further increase occurred. Even with no Ca2+ in the medium, there was still PRL secretion during the incubation. Replacement of Ca2+ with Ba2+ in the medium did not elevate either total PRL levels or PRL release above that in Ca2 +)-free medium. Neither elevated Mg2+ nor increased medium K+ had any effect on PRL synthesis or release. Dopamine inhibited PRL release but not synthesis, as did the D2 receptor agonist, apomorphine. However, the D2 receptor antagonist, (+)-butaclamol was unable to prevent the action of dopamine on PRL release. Somatostatin inhibited both PRL synthesis and release in normal Ca2+ medium, but release only in reduced Ca2+ medium. Thus, Ca2+, dopamine, and somatostatin may all have roles in regulating prolactin secretion in this fish. In addition, oPRL reduced trout PRL release, indicating a possible negative feedback mechanism for trout PRL secretion.

Animals↗
PubMed1983

Irreversible binding of [3H](-)N-chloroethylnorapomorphine to mammalian brain tissue.

A proposed dopamine (DA) receptor labeling agent, [3H](-)N-chloroethylnorapomorphine (3H-NCA) underwent relatively little chemical change at 25 degrees C and pH 6.4 up to an hour of incubation. At low (nM) concentrations it bound rapidly and avidly to a membrane preparation of calf caudate nucleus, but the binding did not saturate over two hours of incubation or at ligand concentrations between 0.2 nM and 10 microM. While similarly bound [3H]-(-)apomorphine was rapidly displaced by DA and other agents that interact with DA receptors, 3H-NCA could not be displaced by unlabeled DA, apomorphine and (+)butaclamol, nor by denaturation of the tissue with trichloracetic acid (TCA). There was no evidence of selectivity of binding of 3H-NCA in regions of rat brain, and binding occurred even to TCA-denatured caudate tissue. Catechol-aporphines prevented binding of 3H-NCA to calf caudate membranes by up to 30%, but this effect was not stereoselective and was lost at concentrations of 3H-NCA above 100 nM. In contrast, DA and ADTN as well as neuroleptics and adrenergic agonists had no such effect. The results suggest that while 3H-NCA may bind irreversibly, and possibly covalently, it does not have high selectivity for labeling dopamine D-3 or D-2 receptor sites, but may be partially selective for an aporphine binding site.

Animals↗
PubMed1989

Evidence for a model of activation of central sigma systems.

Evidence for a drug-induced activation of central sigma systems is presented. The model is the locomotor activation initiated by a subcutaneous (SC) challenge of 1.6 mg/kg of (+)-butaclamol, (+)-BUT, given 30 min before 10 mg/kg SC of (-)-N-allylnormetazocine, (-)-NAN, in Sprague-Dawley male rats which have been pretreated with four daily injections of 10 mg/kg SC of (-)-NAN. The locomotor activation is characterized by an initial 20 min period of retropulsion and sideways-circling followed by 90 to 100 min of forward locomotion. The locomotor syndrome is antagonized by 10 mg/kg of (+/-)-BMY 14802, 20 mg/kg of rimcazole, and 0.2 mg/kg of haloperidol, but not by 0.04 mg/kg of R(+)SCH23390, 100 mg/kg of S(-)sulpiride, 10 mg/kg of naltrexone, or 2.5 mg/kg of MR2266. The data suggest that the manifestation of the (+)-BUT/(-)-NAN-induced syndrome depends upon intact transmission at central sigma sites.

Animals↗
PubMed1990

Evidence for the presence of both D-1 and D-2 dopamine receptors in human esophagus.

Clinical and pharmacological evidence suggested that dopamine is involved in the control of esophageal motility. The present study was designed to determine whether or not dopamine receptors are present in human esophagus. With this aim we measured adenylate cyclase activity as a biochemical index of dopamine receptor function in esophageal specimens taken from five patients during surgery for upper esophageal carcinoma. The selective D-1 agonist fenoldopam stimulated cAMP formation in the lower esophageal sphincter, but not in the esophageal body; this effect was prevented by the selective D-1 antagonist SCH 23390 and by d-butaclamol. Bromocriptine, a selective D-2 stimulator, inhibited adenylate cyclase activity in the lower esophageal sphincter, an effect blocked by the D-2 antagonist (-)sulpiride. No effects of bromocriptine were found in the esophageal body. These data indicate that both D-1 and D-2 receptors are present in the lower esophageal sphincter, but not in esophageal body and emphasize the role of dopamine in the regulation of esophageal function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1978

Dopamine in the hypothalamus of the cat: pharmacological characterization and push-pull perfusion analysis of sites mediating hypothermia.

Within the rostral diencephalon of the cat, 113 sites were examined for their reactivity to 2.33--14.0 microgram dopamine (DA) or 2.33--14.0 microgram norepinephrine (NE) microinjected in a volume of 0.75 microliter. During each experiment, colonic temperature was monitored and additional physiological measures were recorded continuously. In contrast to CSF controls, an intrahypothalamic injection of either catecholamine at circumscribed sites evoked a dose-dependent fall in the cat's body temperature, with NE ordinarily evoking a more profound hypothermic response. The morphological sites of maximum sensitivity were localized in the anterior hypothalamic, preoptic region. At some but not all sites, a prior microinjection of 3.5--7.0 microgram phentolamine attenuated the magnitude of the DA-induced hypothermia and delayed its onset. Conversely, at all loci, the pretreatment by the injection of this alpha-adrenergic antagonist markedly reduced the absolute magnitude of the NE-induced fall in the cat's temperature. Similar pretreatment of a reactive hypothalamic locus with a beta-adrenergic receptor blocking agent, practolol (3.5 microgram), failed to alter the hypothermia following a microinjection of DA. Either of two DA receptor antagonists, haloperidol (0.04--7.0 microgram) or d-butaclamol (0.48--1.47 microgram), when given in a sufficient dose, effectively delayed the onset of the DA-hypothermia and reduced its absolute magnitude; however, the NE-induced decline in the cat's temperature was unaffected by DA receptor blockade. Endogenous stores of DA and/or NE in the cat's hypothalamus were radio-labeled with either 3H- or 14C-catecholamines or both, microinjected through the implanted guide tube into an identified amine-sensitive site. By using push-pull cannulae, the site was subsequently perfused for 5 min with artificial CSF at a rate of 25 microliter/min with samples collected at 15 min intervals. During either the third or fourth perfusion, the ambient temperature of the cat's chamber of 22--24 degrees C was elevated to 35--45 degrees C and maintained at this level for 15 or 30 min. This environmental warming evoked a release of either DA o; NE or both amines from certain circumscribed sites within the cat's rostral hypothalamus. Overall, these results provide pharmacological, physiological and anatomical evidence for a differential role of DA in the hypothalamic mechanism which mediates the heat loss processes.

Animals↗
PubMed1982

Dopamine involvement in ACTH-induced grooming behavior.

Low doses of dopamine agonists and antagonists were tested for their effects on the excessive grooming behavior induced by intracerebroventricular (ICV) injections of ACTH1-24. Grooming scores were significantly depressed at doses of haloperidol, metoclopramide, pimozide, and butaclamol that did not decrease locomotor activity. In fact at two doses of haloperidol (0.067 and 0.10 mg/kg), grooming scores were decreased while locomotor activity was increased significantly. Metoclopramide increased grooming scores at a dose reported to block presynaptic dopamine receptors. Apomorphine potentiated the grooming induced by low doses of ACTH. These data support the hypothesis that dopaminergic neurotransmission is necessary for the display of ACTH-induced grooming behavior.

Adrenocorticotropic Hormone↗
PubMed1983

Evaluation of neurotensin's thermolytic action by ICV infusion with receptor antagonists and a Ca++ chelator.

To investigate the mechanisms responsible for the thermolytic action of neurotensin (NT), cannulae for intracerebroventricular (ICV) injection were implanted stereotaxically in Sprague-Dawley rats. Postoperatively, body temperature in the unrestrained rat was monitored continuously by a colonic thermistor probe. NT in a dose of 1.5-4.5 micrograms or CSF carrier vehicle was infused bilaterally in the cerebral ventricle (ICV) in a volume of 7.5 microliters. With the rats kept at an ambient temperature of 22 degrees C, NT given ICV produced a dose-dependent fall in core temperature of greater than 0.8 degree C. Pre-treatment of the animal's cerebral ventricle with amine receptor antagonists, phentolamine (20.0 micrograms), butaclamol (10.0 micrograms), methysergide (20.0 micrograms) or atropine (25.0 micrograms), all similarly infused ICV, failed to alter the hypothermia induced by NT. However, the calcium chelating agent, EGTA, given ICV in a dose of 4.0-8.0 micrograms blocked the thermolytic effect of NT on body temperature in a concentration-dependent manner. These results suggest that the central thermolytic action of NT is not mediated by catecholamine or other aminergic pathways which are implicated in the central mechanisms of thermoregulation. Rather, the peptide may act on a cellular process involving calcium activity in the hypothalamus, presumably to impair the maintenance of the animal's "set-point" for body temperature.

Animals↗
PubMed1991

Monoaminergic regulation of proopiomelanocortin messenger RNA concentrations in primary cell cultures of rat hypothalamus.

The effect of monoaminergic neurotransmitters on a 1.1-kb proopiomelanocortin messenger RNA (POMC mRNA) detected in rat hypothalamic cells maintained in culture has been evaluated. Serotonin caused a 15% increase in POMC mRNA levels, an effect which was blocked by the 5-HT2 receptor antagonist ketanserin. Dopamine markedly decreased POMC mRNA levels in a dose related manner. Haloperidol and the selective D2 antagonist (+)-butaclamol prevented the inhibitory effects of both dopamine and the selective D2 agonist, 2-bromo-alpha-ergocryptine. The selective dopamine D1 receptor agonist, SKF 38393, as well as norepinephrine and acetylcholine did not affect POMC mRNA levels. It is concluded that serotonin exerts a positive control and dopamine a negative control on POMC mRNA concentrations in primary cultures of rat hypothalamic neurons. The negative effect of dopamine appears to be exerted via D2 receptor-mediated mechanism.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1984

Prolactin secretion by cultured anterior pituitary cells: influence of culture conditions and endocrine status of the pituitary donor.

The characteristics of prolactin (PRL) secretion by cultured anterior pituitary cells in the presence and absence of catecholamines were studied. PRL secretion was markedly influenced by culture conditions such as cell density, culture duration and length of short-term incubation. Dopamine (DA) inhibited PRL release in a dose-dependent manner within a physiological range, and this inhibition was reversed by the stereospecific DA receptor antagonist (+)-butaclamol. In contrast, the inhibition of PRL secretion by norepinephrine (NE) required much higher doses and lacked specificity. Cells obtained from male donors had the lowest basal PRL secretion and were the least responsive to DA inhibition, whereas those obtained from females in late pregnancy had the highest basal PRL secretion and were the most sensitive to DA.

Animals↗
PubMed1981

[3H]Spiroperidol binding in normal and denervated carotid bodies.

Specific dopamine receptors were studied in freshly dissected, unhomogenized rabbit carotid bodies incubated in [3H]spiroperidol. Total binding and non-specific binding were determined in the absence and presence of 0.2 microM (+)-butaclamol, respectively. Specific binding in normal carotid bodies incubated at near saturating concentrations (0.38 nM) was 1.63 +/- 0.58 pmol/g of tissue. Chronic section of the carotid sinus nerve (14 days) resulted in a 64% reduction (P less than 0.05) in specific binding. We conclude that the majority of specific dopaminergic receptors are located on carotid sinus nerve afferent terminals.

Animals↗
PubMed1986

The relaxing effect of SKF 38393 on the catch contraction of Mytilus smooth muscle.

The relaxing effect of SKF 38393 on the catch contraction in the anterior byssus retractor muscle (ABRM) of Mytilus and the effect of SKF 38393 on the cyclic AMP (cAMP) levels in the ABRM were investigated. The catch contraction was relaxed by SKF 38393 in a dose-dependent manner. The dose-response curves of SKF 38393 were shifted in parallel to the right by butaclamol (3 X 10(-6) and 6 X 10(-6) M) and haloperidol (3 X 10(-6) and 3 X 10(-5) M). Their pA2 values were 5.69 +/- 0.05 and 5.80 +/- 0.07. The cAMP levels in the ABRM were not altered by SKF 38393 at a concentration (10(-5) M) sufficient to relax. These findings indicate that the dopamine receptors of the ABRM are D-1 like receptors but somewhat different from those of the vertebrates.

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