Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Butaclamol”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed1985

Dopamine D-2 receptors in rat caudate-putamen: the lateral to medial gradient does not correspond to dopaminergic innervation.

The topography of dopamine D-2 receptors within the rat caudate-putamen (CPU) was characterized by measuring [3H]spiroperidol binding to membranes from dissected regions of the CPU and to thin sections of rat forebrain using quantitative autoradiography. Specific binding, defined using 1 microM (+)-butaclamol, was considerably higher in the lateral CPU than the medial CPU, without any obvious gradient in the dorsoventral axis. The difference in Bmax between the lateral and medial CPU was similar whether determined by digital subtraction autoradiography of coronal forebrain sections or by [3H]spiroperidol binding to membrane homogenates derived from CPU subregions. No regional differences were observed in the affinity of [3H]spiroperidol for D-2 sites. There were no lateral-to-medial differences in the dopaminergic innervation of the CPU, as determined by the measurement of the levels of dopamine, homovanillic acid and dihydroxyphenylacetic acid in subregions of the CPU using high pressure liquid chromatography. Thus, regional variations in the density of D-2 receptors within the CPU do not correspond to the degree of dopaminergic innervation. The functional importance of the organization of this dopamine receptor system is discussed in relation to the lateral-to-medial organization of the CPU.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Dopaminergic regulation of GABA release from the intact goldfish retina.

The rate of release of [3H]GABA from intact goldfish retinas was studied using a modified superfusion technique. Small, significant increases in the rate of GABA release were observed when the retinas were exposed to dopamine (DA) (100-1000 microM); however, when free Ca2+ was removed from the medium, the basal rate of GABA release was increased and DA became inhibitory. Forskolin, a non-specific stimulator of adenylate cyclase in intact cells, also inhibited GABA release in the absence of Ca2+. There was no significant effect of forskolin in the presence of Ca2+; however, (+)-butaclamol, a dopamine antagonist, increased basal GABA release under these conditions. L-glutamic acid (L-Glu) (1-10 mM) causes up to a 10-fold increase in GABA release. In the presence of Ca2+, DA did not significantly alter the effects of L-Glu; however, in the absence of Ca2+ a significant inhibition of the effects of L-Glu by DA was observed. Forskolin, on the other hand, inhibited the effects of L-Glu both in the presence and absence of Ca2+. Finally, EGTA (0.3-1 mM) produced a large release of GABA: this release was inhibited by DA, forskolin, theophylline, and 8-bromo cyclic AMP. These results suggest a model wherein DA stimulates Ca2+-dependent GABA release from one site and inhibits Ca2+-independent GABA release from another site via a cyclic AMP-mediated event.

Animals↗
PubMed1986

Characterization of dopamine receptors on neurons grown in primary dissociated cell culture from ventral mesencephalon of mouse.

Mammalian neurons from ventral mesencephalon were grown in primary dissociated cell culture. These cultures were examined for dopamine sensitive adenylate cyclase activity and specific ligand binding of [3H]spiroperidol and [3H]flupenthixol. No stimulation of adenylate cyclase activity by 10 microM dopamine was demonstrable in cell culture homogenates. [3H]Spiroperidol bound to cell culture homogenates with high affinity and was displaced by (+)-butaclamol but not by 5-hydroxytryptamine, suggesting that the [3H]spiroperidol was bound to dopamine receptors. While [3H]flupenthixol binding was also present, it could be displaced by spiroperidol indicating that the dopamine receptor was probably of the D2 subtype. Binding of spiroperidol was proportional to the amount of cell culture homogenate, and was saturable. Are these receptors autoreceptors? The toxin 1-methyl-4-phenylpyridine (MPP+) was used to destroy dopaminergic neurons; spiroperidol binding in these cultures was found to be increased, demonstrating that most of these D2 receptors are not autoreceptors.

1-Methyl-4-phenylpyridinium↗
PubMed1987

Effects of sulpiride and apomorphine on prolactin release in adrenalectomized animals. Role of sodium ions.

The present experiments were performed to demonstrate in vivo the existence of a modulatory role of Na+ in the inhibitory control of prolactin (PRL) secretion. Groups of adult male rats were either adrenalectomized (adrenex) or sham-operated (normals) and implanted in the right atrium with a chronic cannula for the infusion of solutions or the sequential withdrawal of blood samples. Four days later, adrenex rats were infused for 1 h with either saline 0.9% or dextrose 5.6% (310 mOsm/kg H2O) at the rate of 10 ml/kg/h from Time -60 min until Time 0 min. All animals were injected at Time -45 min with sulpiride 0.05 mg/kg. At Time 0 min, some animals received apomorphine 5 mg/kg while others received a 0.05 mg/kg dose of the drug. Blood samples were obtained at -45, -30, -15, 0, 5, 10, 20 and 30 min for PRL assay. Plasma Na+ concentration was measured at -45, 0 and 30 min and plasma osmolarity at 0 min in adrenex rats. In normal controls plasma Na+ values were measured at the end of the experiment. Binding values (KD and Bmax) of pituitary D2-receptors were measured in adrenex and sham-operated rats using [3H]spiroperidol as ligand and D-butaclamol to define non-specific binding. Plasma Na+ values remained constant in saline-infused adrenex rats and similar to those of normal controls, while in dextrose-infused adrenex rats they fell progressively during the experimental period and were always lower than in the two other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1991

Multiple fluorescent ligands for dopamine receptors. II. Visualization in neural tissues.

Selective dopamine receptor ligands, (R,S)-5-(4'-aminophenyl)-8-chloro-2,3,4, 5-tetrahydro-3-methyl-[1H]-3-benzazepin-7-ol, the 4'-amino derivative of the high affinity D1 receptor antagonist SCH 23390, the high affinity D2 receptor antagonist N-(p-aminophenethyl)-spiperone or NAPS, and the D2 selective agonist, 2-(N-phenethyl-N-propyl)-amino-5-hydroxytetralin or PPHT were chemically coupled to the fluorescent compounds, Bodipy, Cascade blue, coumarin, fluorescein, rhodamine, or Texas red. The utility of the 6 fluorescent moieties linked to the 3 dopamine receptor binding ligands for anatomical study of regional and cellular distribution patterns of the two dopaminergic receptor subtypes has been assessed in frozen sections of the rat striatum and compared to our previous report using the rhodamine-labeled antagonists. The regional staining for the two dopaminergic receptor binding sites supports previous work using in vitro receptor autoradiographic analyses; the D1 receptor binding was more robust than that of D2 receptors in the caudate nucleus. The cellular element which most frequently expressed striatal D1 binding sites had a medium-diameter cell body. Medium-sized cells also exhibited fluorescence for the D2 binding site, as did a much larger diameter element; potentially the cholinergic interneuron of the caudate nucleus. The pharmacological specificity for each of the different D1 fluorescent antagonist ligands in the tissues was determined by competition with 100-fold excess of unlabeled SCH 23390 (non-specific binding), spiroperidol (binding selectivity), the stereoactive paired isomers of butaclamol, and the serotonin 5-HT2 receptor antagonist ketanserin. The same criteria were used to assess the different D2 fluorescent agonist and antagonist ligand derivatives. The anatomical efficacy of these novel ligands was determined using selective dichroic filters to stimulate the fluorescent moieties in the optimal excitation wavelength, and the amount of fluorescent dopamine receptor binding was photographically measured and contrasted for each of the newly synthesized fluoroprobes. Using the most pharmacologically specific and anatomically efficient of these novel fluoroprobes, we determined the localization pattern of the D1 and D2 dopamine receptor binding sites in tissues reported to exhibit both subtypes of the receptor. The cellular distribution of the dopamine receptor binding sites was determined concurrently using fluoroprobes in the forebrain, mesencephalon, pituitary, retina, and superior cervical ganglion of the rodent, and bovine adrenal medullary chromaffin cells were examined using the rhodamine-labeled antagonists.

Adrenal Medulla↗
PubMed1994

In vivo treatment with mu and delta, but not kappa-selective opioid agonists reduces [3H]spiperone binding to the guinea-pig striatum: autoradiographic evidence.

In guinea-pigs, acute treatment with mu and delta receptor opioid agonists induces sedation and immobility [1,5], and attenuates the behavioural activation produced by the dopamine D2 agonist quinpirole [5]. In contrast, kappa-selective opioid agonists induce dystonic-like movements [4,5,8]. This has led us to investigate the possibility of an interaction between acute opioid treatment and the dopamine D2 system. The effect of acute treatment with mu, delta and kappa opioid agonists on [3H]spiperone binding sites (dopamine D2) in guinea-pig brain was studied using receptor autoradiography. The mu preferring agonist morphine (15 mg/kg subcutaneously, SC) given for 2 h, and the delta receptor selective agonist DPDPE (Tyr-D-Pen-Gly-Phe-D-Pen) (20 nM, intracerebroventricularly, ICV) given for 0.5 h, both decreased the density of specific (butaclamol displaceable) [3H]spiperone binding in the caudate putamen by 23.8 +/- 1.7% and 24.2 +/- 2.7% respectively, and in nucleus accumbens by 26.1 +/- 2.7% and 21.9 +/- 4.6% respectively compared to saline treated animals. There were no significant changes in the level of [3H]spiperone binding to other brain regions examined including frontal cortex, hippocampus, substantia nigra, ventral tegmental area, amygdala, hypothalamic nuclei and cerebellum. In other experiments, incubation of coronal slices from various brain regions with [3H]spiperone, in the presence of a high concentration of morphine (20 microM) or DPDPE (10 microM) did not affect the level of binding, thus precluding effects due to residual tissue levels of drugs after in vivo treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1995

Dopamine D2-like receptors labeled by [3H]YM-09151-2 in the rat hippocampus: characterization and autoradiographic distribution.

Dopamine D2-like receptor labeled by [3H]YM-09151-2 in the rat hippocampus proper was examined by in vitro receptor autoradiography. In the dorsal hippocampus, [3H]YM-09151-2 bindings were high in the whole layers of CA1, the stratum pyramidale of CA4 and the stratum molecular of gyrus dentatus, moderate in the stratum oriens of CA3 and hilus of the gyrus dentatus, and low in remaining CA3 and the subiculum. In the ventral hippocampus, the binding densities were high in the stratum oriens and the stratum radiatum of CA1, the stratum pyramidale of CA4, and the stratum moleculare of gyrus dentatus, moderate in the stratum lacnosum moleculare of CA1 and the hilus of the gyrus dentatus. Saturation analysis using hippocampal sections demonstrated that the Kd value was about five times higher than that using striatal sections. The rank order potency of competition on [3H]YM-09151-2 binding by dopaminergic ligands in the hippocampus was YM-09151-2 > (+)-butaclamol > dopamine > sulpiride > SCH-23390; which shows the appropriate dopamine D2-like receptor profile. The hippocampal [3H]YM-09151-2 binding did not represent serotonergic receptors (5-HT1A and 5-HT2) and sigma receptor, since Ki values of ketanserine, serotonin, 8-OH-DPAT and DTG were much lower than D2-like receptor antagonists. These findings suggest tha [3H]YM-09151-2 binds hippocampal D2-like receptor site with different association kinetics of striatal D2-like receptor site, and demonstrates widespread distribution of D2-like receptor in the hippocampus with distinct region-specific profile.

Animals↗
PubMed1996

Localization of D1 dopamine receptors on live cultured striatal neurons by quantitative fluorescence microscopy.

Single neurons in culture express a heterogeneity of neurotransmitter receptor subtypes. The study of the effects of neurotransmitters on neuronal function is complicated by this heterogeneity. It would therefore be useful to be able to identify live neurons that express the receptors of interest and then use these neurons for functional studies. We have used quantitative fluorescence microscopy to identify single live striatal neurons that express D1 dopamine receptors. The binding of the fluorescent D1 dopamine receptor antagonist bodipy-SCH 23390 was measured in 2-3-week-old primary striatal cultures derived from fetal rats (embryonic day 18). Binding of bodipy-SCH 23390 to live neurons was displaced by (+)-butaclamol, dopamine or SCH 23390, indicating that it specifically labelled D1 dopamine receptors. However, the fraction of bodipy-SCH 23390 binding that was specific varied substantially among individual neurons indicating heterogeneity of D1 dopamine receptor expression. Interestingly, bodipy-SCH 23390 also specifically labelled discrete spots of receptors on the neuronal processes. This technique should prove useful in the study of the effects of dopaminergic drugs on neuronal function in primary culture.

Acids↗
PubMed1978

Antagonism of central histamine H1 receptors by antipsychotic drugs.

The activity of 8 widely antipsychotic drugs as antagonists of central histamine H1 receptors was determined from the inhibition of the binding of 3H-mepyramine to a membrane fraction from guinea-pig brain. The phenothiazines examined, clorpromazine, fluphenazine, thioridazine and trifluoperazine, were all potent H1 antagonists. Both alpha- and beta-flupenthixol were potent inhibitors, but butaclamol, although less potent, showed stereospecificity. Haloperidol and spiperone were markedly weaker antihistamines than the phenothiazines.

Animals↗
PubMed1979

Dopamine agonist-induced hyperglycemia in rats: effects of lergotrile mesylate.

Lergotrile and apomorphine, two direct-acting dopamine agonists, caused marked hyperglycemia in fasted rats, while compounds which release endogenous dopamine (amphetamine, methylphenidate) or inhibit dopamine reuptake (LR5182), failed to elevate blood glucose. The effect of lergotrile was dose dependent, causing blood glucose to rise 3-fold above resting levels at 5 mg/kg (i.p.). Blood glucose increased prior to the onset of the behavioral signs of dopamine stimulation. The effect of lergotrile was attenuated by phentolamine, propranolol or butaclamol. Adrenalectomy also prevented lergotrile-induced hyperglycemia. These data indicate that hyperglycemia is not a property of all compounds that cause dopaminergic effects. The action of lergotrile might be indirect, perhaps mediated through release of catecholamines from the adrenal glands.

Adrenalectomy↗
PubMed1982

Dopaminergic effects on tail-flick response in spinal rats.

R-Apomorphine (0.02-1.75 mumol/kg), administered by intrathecal infusion to spinalized rats, caused a dose-dependent increase in tail-flick latency. The effect of R-apomorphine was counteracted significantly by the dopaminergic receptors antagonists cis-flupenthixol (0.20-3.94 mumol/kg) and (+)-butaclamol (0.78 mumol/kg), but not by their enantiomers nor by phenoxybenzamine (29.40 mumol/kg) or methysergide (29.40 mumol/kg). The findings suggest that dopaminergic mechanisms play a role in the modulation of nociception in the spinal cord.

Animals↗
PubMed1983

Dopamine receptors in human basilar arteries.

After phenoxybenzamine (10(-5) M), pretreatment, and in the presence of propranolol (10(-6) M) and indomethacin (2.8 X 10(-6) M), dopamine caused a marked concentration-dependent relaxation of isolated strips of human basilar artery contracted with PGF2 alpha. This effect was mimicked by apomorphine, 6,7-ADTN and SK&F 38393, but N,N-diethyl dopamine, N,N-di-n-propyl-dopamine and 5,6-ADTN caused only slight relaxation. (+)-Butaclamol, cis-alpha-flupenthixol, fluphenazine and haloperidol competitively antagonised the relaxant effects of dopamine, but sulpiride was ineffective in concentrations as high as 1.3 X 10(-4) M. These findings show that the dopamine receptors in the human basilar artery closely resemble those in the smooth muscle of the rabbit isolated mesenteric and splenic arteries, and the dog renal and mesenteric arteries in vivo, but differ from those located presynaptically on sympathetic nerve terminals.

Basilar Artery↗
PubMed1983

Interactions of neuroleptic compounds at alpha 2-adrenergic receptor affinity states in bovine caudate nucleus.

Several recent studies have suggested a connection between neuroleptics and/or dopamine systems, and alpha 2-adrenergic receptors. Competition of a variety of neuroleptics at specific alpha 2-adrenergic binding sites (labeled with [3H]rauwolscine or [3H]p-aminoclonidine) in bovine caudate and cortex was examined. Few of the compounds were potent competitors, with (+)-butaclamol, alpha-flupenthixol, clozapine and pimozide the most potent (IC50 range 100-600 nM), while triflupromazine, mesoridazine, and haloperidol were the least potent (IC50 range 5 000-10 000 nM). These findings indicate that few, if any, of the examined neuroleptics have specific, high-affinity interactions with the multiple affinity states of the alpha 2-adrenergic receptor.

Animals↗
PubMed1985

Kinetic and pharmacological profiles of the in vitro binding of the potent dopamine agonist [3H]N,N-dipropyl-5,6-dihydroxy-2-aminotetralin to rat striatal membranes.

The in vitro binding of the new tritiated dopaminergic ligand [3H]N,N-dipropyl-5,6-dihydroxy-2-aminotetralin to rat striatal membranes is described. Binding assays were performed in 50 mM Tris-HCl pH 7.5 containing 1 mM EDTA and 0.01% ascorbic acid at 25 degrees C for 30 min. Specific binding at 0.5 nM [3H]DP-5,6-ADTN and 5 mg/ml membrane suspension was very high (87-93%) and was found to be linearly related with homogenate concentration over the range of 0.5-10 mg/ml (r = 0.9968). (+)Butaclamol 1 microM was used to define specific binding. Specific binding disappeared completely within 20 min when the tissue was incubated at 55 degrees C. Association and dissociation curves (obtained after addition of 1 microM (-)-DP-5,6-ADTN) were converted to linear logarithmic plots and the kinetic constants were computed (k1 = 0.054 min-1 and k-1 = 0.0188 min-1) as were the t1/2 for association (3.52 min) and dissociation (20.8 min). This resulted in an apparent KD of 0.34 nM. Increasing concentrations of [3H]DP-5,6-ADTN (0.05-3.0 nM) were found to saturate the receptor site. Linear transformation of the saturation curves and presentation of the curves as Eadie-Hofstee plots showed that only one set of receptors was labeled (nHill was 0.995 +/- 0.07) with a high affinity constant KD of 0.57 +/- 0.10 nM and a maximum number of binding sites Bmax of 18.6 +/- 2.4 pmol/g tissue. Various compounds were tested for their potency to displace the specific binding of [3H]DP-5,6-ADTN to striatal membranes (2.5 mg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The effect of different types of cortical lesions on drug-induced catalepsy in rats: a pharmacological analysis.

The effect of bilateral lesions of various cortical areas on neuroleptic- and non-neuroleptic-induced catalepsy was studied in the rat. Ablation of the frontal or parietal cortex led to a marked decrease in haloperidol catalepsy, whereas lesions of the occipital cortex, or of the olfactory bulbs did not affect catalepsy, when measured 3 weeks post lesion in all cases. The frontal cortex lesions also diminished the cataleptic state induced by cis-flupenthixol, (+)-butaclamol and chlorpromazine, but failed to affect that induced by reserpine, tetrabenazine or morphine. Four months after the frontal lesions, haloperidol catalepsy was at control values, and a rebound phenomenon was observed at 10 months post lesion. The homeostatic mechanisms seem to have stabilized at 18 months post lesion when haloperidol catalepsy had returned to control levels.

Animals↗
PubMed1986

The St 587-induced flexor reflex in pithed rats: a model to evaluate central alpha 1-receptor blocking properties.

A combination of reserpine, nialamide and the specific alpha 1-adrenoceptor agonist St 587 [2-(2-chloro-5-trifluoromethylphenylimino)-imidazolidine] induced a marked increase of the electrically stimulated flexor reflex in pithed rats. This increased reflex - which lasted for more than 3 h - could be inhibited by the alpha 1-receptor antagonist prazosin but not by the alpha 2-adrenoceptor antagonist idazoxan (RX 781094). A range of different drugs was tested, including 17 neuroleptics. Most of the neuroleptics showed marked inhibition of the St 587-induced reflex. Bromperidol, butaclamol and fluperlapine were weak inhibitors while pimozide was without effect. The results showed close correlation to alpha 1-receptor affinities in vitro (r = 0.84, P less than 0.001) while no correlation was found to either D-2 receptor affinities or to 5-HT2 receptor affinities in vitro (r = 0.43, P less than 0.2 and r = 0.41, P less than 0.05, respectively). It is concluded that inhibition of the St 587-induced flexor reflex in pithed rats is an in vivo test model for central alpha 1-receptor blocking properties.

Adrenergic alpha-Antagonists↗
PubMed1986

Stereoselective inhibition of prolactin secretion by (-)-HW-165, a novel 3-PPP congener; further support for similarities between central DA autoreceptors and pituitary lactotroph DA receptors.

The novel atypical dopamine (DA) receptor agonist HW-165 (trans-7-hydroxy-1,2,3,4,4a,5,6,10b-octahydrobenzo(f)quinoline), a 'rigid' 3-PPP congener, and its enantiomers were investigated with regard to their actions on prolactin (PRL) release in rats. Racemic HW-165 dose dependently inhibited the elevation of PRL secretion induced by monoamine synthesis disruption (NSD 1015) combined either with abolished DA nerve impulse flow (GBL) or with monoamine depletion (reserpine). Racemic HW-165 was roughly equipotent to 3-PPP but 5-10-fold less potent than apomorphine. The PRL inhibitory action of racemic HW-165 was stereoselectively prevented by the DA antagonist (+)-butaclamol. Since the chiral aspect of lactotroph DA receptor activation by 'atypical' DA receptor agonists has not been covered in previous investigations the effects of the HW-165 enantiomers were now studied. Our findings suggest that the PRL inhibitory properties of racemic HW-165 reside in its (-) enantiomer, (+)-HW-165 being devoid of activity. Taken together, the results reinforce the concept that the pituitary lactotroph DA receptors mediating the inhibition of PRL release are similar, notably also from a stereochemical point of view, to central DA receptor sites with presumed high agonist sensitivity, such as DA autoreceptors.

4-Butyrolactone↗
PubMed1988

Comparison of the pharmacological characteristics of [3H]raclopride and [3H]SCH 23390 binding to dopamine receptors in vivo in mouse brain.

In vivo binding of the benzamide derivative [3H]raclopride was studied in mouse brain. The binding was saturable, reversible and stereospecific. Non-specific binding was 5-15% of the total binding. Pharmacological characterization of the binding indicated labelling of dopamine D2 receptors since the binding was potently inhibited by compounds with high affinity for this receptor in vitro. On the other hand, compounds with low affinity in vitro i.e., dopamine D1-selective compounds were weak or inactive as inhibitors of [3H]raclopride binding. A comparison of the pharmacological characteristics of [3H]raclopride and [3H]SCH 23390 binding in vivo indicated that compounds with selectivity in vitro retained this selectivity in vivo. Thus, spiroperidol, haloperidol, 1-sulpiride, clebopride, LY 171555 and (-)-NPA ((-)-N-propyl-norapomorphine) were D2 selective while SCH 23390, SKF 38393 and SKF 75670 were D1 selective. Clozapine, tilozepine, cis-flupentixol, chlorpromazine and butaclamol were non-selective both in vitro and in vivo. However, a few compounds changed profile in vivo compared to in vitro. Thus, fluperlapine and fluphenazine had a dual D1-D2 receptor profile in vitro but were D1- or D2-selective in vivo, respectively. Pergolide and molindone which were D2-selective in vitro both had a dual D1-D2 receptor profile in vivo. In conclusion, [3H]raclopride, in vivo, selectively labels the dopamine D2 receptor. Comparison of the pharmacological characteristics of [3H]raclopride and [3H]SCH 23390 binding in vivo supported the that the dopamine D1 receptor is an important target for a variety of neuroleptics, especially of the clozapine type. This may indicate that blockade of the dopamine D1 receptor conveys antipsychotic action.

Animals↗