A benzocycloheptapyridoisoquinolinol that has been used as an antipsychotic, especially in schizophrenia.
Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.

Real-time analysis of dopamine: antagonist interactions at recombinant human D2long receptor upon modulation of its activation state. (1/27)

1. Antipsychotic drugs may mediate their therapeutic effects not only by preventing the binding of dopamine but also by decreasing the propensity of the dopamine receptor to assume an active R* state. Ligand-mediated activation and blockade of the recombinant human D(2long) receptor was investigated in CHO-K1 cells upon modulation of its R* state. 2. Both the Ala(371)Lys (A371K) and Thr(372)Arg (T372R) D2long receptor mutants could be activated in a ligand-dependent manner via a chimeric G(alphaq/o) protein, and more efficaciously so than with the promiscuous G(alpha15) protein. 3. Dopamine and partial agonists (E(max): lisuride >> (+)-UH 232 approximately bromerguride) displayed dissimilar Ca(2+) kinetic properties at wild-type and mutant receptors. A371K and T372R D2long receptor mutants demonstrated an attenuated and enhanced maximal response to these partial agonists, respectively. 4. Dopamine antagonists were unable to block the transient high-magnitude Ca(2+) phase at the wild-type D2long receptor upon simultaneous exposure to antagonist and dopamine, while full blockade of the low-magnitude Ca(2+) phase did occur at a later time (onset-time: haloperidol < bromerguride < (+)-butaclamol). A similar, though more efficacious, antagonist profile was also found at the A371K mutant receptor. Conversely, the blockade of the low-magnitude Ca(2+) phase was attenuated (haloperidol) or almost absent [(+)-butaclamol and bromerguride] at the T372R mutant receptor. 5. In conclusion, mutagenesis of the Ala(371) and Thr(372) positions affects in an opposite way the ligand-dependent activation and blockade of the D2long receptor. The observed attenuation of dopamine-mediated Ca(2+) signal generation with different decay-times may underlie distinct properties of the dopaminergic ligands.  (+info)

Dopamine receptor oligomerization visualized in living cells. (2/27)

G protein-coupled receptors occur as dimers within arrays of oligomers. We visualized ensembles of dopamine receptor oligomers in living cells and evaluated the contributions of receptor conformation to the dynamics of oligomer association and dissociation, using a strategy of trafficking a receptor to another cellular compartment. We incorporated a nuclear localization sequence into the D1 dopamine receptor, which translocated from the cell surface to the nucleus. Receptor inverse agonists blocked this translocation, retaining the modified receptor, D1-nuclear localization signal (NLS), at the cell surface. D1 co-translocated with D1-NLS to the nucleus, indicating formation of homooligomers. (+)-Butaclamol retained both receptors at the cell surface, and removal of the drug allowed translocation of both receptors to the nucleus. Agonist-nonbinding D1(S198A/S199A)-NLS, containing two substituted serine residues in transmembrane 5 also oligomerized with D1, and both were retained on the cell surface by (+)-butaclamol. Drug removal disrupted these oligomerized receptors so that D1 remained at the cell surface while D1(S198A/S199A)-NLS trafficked to the nucleus. Thus, receptor conformational differences permitted oligomer disruption and showed that ligand-binding pocket occupancy by the inverse agonist induced a conformational change. We demonstrated robust heterooligomerization between the D2 dopamine receptor and the D1 receptor. The heterooligomers could not be disrupted by inverse agonists targeting either one of the receptor constituents. However, D2 did not heterooligomerize with the structurally modified D1(S198A/S199A), indicating an impaired interface for their interaction. Thus, we describe a novel method showing that a homogeneous receptor conformation maintains the structural integrity of oligomers, whereas conformational heterogeneity disrupts it.  (+info)

Prototypical antipsychotic drugs protect hippocampal neuronal cultures against cell death induced by growth medium deprivation. (3/27)

BACKGROUND: Several clinical studies suggested that antipsychotic-based medications could ameliorate cognitive functions impaired in certain schizophrenic patients. Accordingly, we investigated the effects of various dopaminergic receptor antagonists--including atypical antipsychotics that are prescribed for the treatment of schizophrenia--in a model of toxicity using cultured hippocampal neurons, the hippocampus being a region of particular relevance to cognition. RESULTS: Hippocampal cell death induced by deprivation of growth medium constituents was strongly blocked by drugs including antipsychotics (10(-10)-10(-6) M) that display nM affinities for D2 and/or D4 receptors (clozapine, haloperidol, (+/-)-sulpiride, domperidone, clozapine, risperidone, chlorpromazine, (+)-butaclamol and L-741,742). These effects were shared by some caspases inhibitors and were not accompanied by inhibition of reactive oxygen species. In contrast, (-)-raclopride and remoxipride, two drugs that preferentially bind D2 over D4 receptors were ineffective, as well as the selective D3 receptor antagonist U 99194. Interestingly, (-)-raclopride (10(-6) M) was able to block the neuroprotective effect of the atypical antipsychotic clozapine (10(-6) M). CONCLUSION: Taken together, these data suggest that D2-like receptors, particularly the D4 subtype, mediate the neuroprotective effects of antipsychotic drugs possibly through a ROS-independent, caspase-dependent mechanism.  (+info)

Serotonin transduction cascades mediate variable changes in pyloric network cycle frequency in response to the same modulatory challenge. (4/27)

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Cuticular plasticization in the tick, Amblyomma hebraeum (Acari: Ixodidae): possible roles of monoamines and cuticular pH. (5/27)

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Dopamine D2 receptors in the rat brain: autoradiographic visualization using a high-affinity selective agonist ligand. (6/27)

The non-catechol, selective dopamine D2-agonist compound 3H-205-502 was used to localize dopamine D2 receptors by autoradiography after in vitro labeling of brain sections. The characteristics of the binding of this ligand to tissue sections were those expected from the labeling of dopamine D2 receptors. The binding of 3H-205-502 was inhibited selectively and stereospecifically by dopamine D2 agents but not by dopamine D1 compounds. The autoradiographic localization of 3H-205-502 binding sites showed high densities of dopamine D2 receptors in areas such as the glomerular layer of the olfactory bulb, the nucleus accumbens, caudate-putamen, olfactory tubercle, the lateral septum, and the islands of Calleja. Besides these dopamine-innervated areas the substantia nigra and the ventral tegmental area also showed important receptor densities. Other areas where dopamine D2 receptor binding was found were the stratum lacunosum-moleculare of the hippocampus, bands of labeling in the molecular layer of the 9th and 10th lobules of the cerebellum, and several components of the visual system. This distribution presents similarities and differences with previously reported distributions of dopamine D2 receptors visualized autoradiographically using 3H-labeled agonists and antagonists. In view of the high affinity, guanine nucleotide insensitivity, and dopamine D2 selectivity of this agonist ligand, it is suggested that dopamine D2 receptors exist in different states in different areas. 3H-205-502 appears to be a new and useful tool for the study of dopamine D2 receptors.  (+info)

Characterization of binding sites for 3H-spiroperidol in human retina. (7/27)

Binding sites for the D-2-selective antagonist (3H)-spiroperidol were characterized in human retina. Nonspecific binding, measured in the presence of 2 microM (+)-butaclamol, made up 20% of total binding. Scatchard analysis of the binding of (3H)-spiroperidol resulted in linear plots and yielded a Kd value of 87 pM and a Bmax value of 1500 fmol/mg protein. In studies of the inhibition of the binding of (3H)-spiroperidol, (+)-butaclamol was approximately 1000-fold more potent than the (-)-stereoisomer. The inhibition curve for dopamine was shifted to the right and the Hill coefficient was increased by the addition of 300 microM GTP. This effect was agonist-specific and suggests that some of the receptors are coupled to stimulation or inhibition of the enzyme adenylate cyclase. The inhibition curves for most of the antagonists had Hill coefficients between 0.6 and 0.8. Hill coefficients were also consistently less than 1.0 for agonists even in the presence of GTP. Nonlinear regression analysis of untransformed data revealed that these shallow inhibition curves were best explained by the presence of two populations of binding sites, 40% of the sites having a high affinity for dopamine in the presence of GTP and domperidone and the remaining 60% having a lower affinity for these ligands. The larger population of sites had a higher affinity for sulpiride, fluphenazine, and N-propylnorapomorphine in the presence of GTP. The possibility that either of these classes of sites consisted of serotonin receptors was ruled out by the finding that the 5-HT2 antagonist ketanserin had a low affinity for both classes of sites.  (+info)

Modulation of cone horizontal cell activity in the teleost fish retina. II. Role of interplexiform cells and dopamine in regulating light responsiveness. (8/27)

Following the destruction of the terminals of the dopaminergic interplexiform cells by intraocular injections of 6-hydroxydopamine (6-OHDA), cone horizontal cells exhibited high light responsiveness in prolonged darkness and their responses to moderate and bright full-field flashes were as large as 60 mV. Furthermore, the light responsiveness of these cells in the 6-OHDA-treated retinas was not enhanced by background illumination. The application of dopamine (50 microM) by superfusion to 6-OHDA-treated retinas resulted in a decrease in light responsiveness and changes in response waveform of the cone horizontal cells. Twenty minutes following dopamine application the responses of the cone horizontal cells closely resembled the response of cells recorded in prolonged dark-adapted retinas. Dopamine caused similar changes in cone horizontal cells recorded in light-exposed retinas, but had no obvious effects on rod horizontal cells. The selective dopamine D1 receptor antagonist, Sch 23390, enhanced cone horizontal cell responsiveness when applied to prolonged dark-adapted retinas, mimicking background illumination. The light responsiveness of cone horizontal cells recorded after application of Sch 23390 was less than that for cells in retinas that had been exposed to background lights, but light responsiveness could not be further enhanced by background illumination. Another dopamine antagonist, (+)-butaclamol, was found to have effects similar to Sch 23390 on cone horizontal cells, but (-)-butaclamol, the inactive enantiomer, did not enhance the light responsiveness of these cells. The results suggest that the dopaminergic interplexiform cells play a crucial role in the regulation of cone horizontal cell responsiveness by prolonged darkness and background illumination. These cells may release dopamine tonically in the dark, which suppresses cone horizontal cell responsiveness. Background illumination may decrease dopamine release and liberate cone horizontal cells from the suppression.  (+info)

Butaclamol is a type of antipsychotic drug that is used primarily in research settings. It is not commonly used in clinical practice due to its significant side effects.

Chemically, butaclamol is a derivative of haloperidol, another antipsychotic medication. It works as an antagonist at dopamine receptors in the brain, particularly at the D1 and D2 receptor subtypes. This can help to reduce the symptoms of psychosis, such as delusions and hallucinations, although other antipsychotics are typically preferred due to their more favorable side effect profiles.

In addition to its use in research, butaclamol has been investigated for its potential therapeutic benefits in a range of conditions, including substance abuse disorders, Tourette's syndrome, and chronic pain. However, further research is needed to establish its safety and efficacy in these contexts.

It is important to note that butaclamol should only be used under the close supervision of a healthcare provider, and its use is typically reserved for cases where other treatments have been ineffective or are not well-tolerated.

Dopamine receptors are a type of G protein-coupled receptor that bind to and respond to the neurotransmitter dopamine. There are five subtypes of dopamine receptors (D1-D5), which are classified into two families based on their structure and function: D1-like (D1 and D5) and D2-like (D2, D3, and D4).

Dopamine receptors play a crucial role in various physiological processes, including movement, motivation, reward, cognition, emotion, and neuroendocrine regulation. They are widely distributed throughout the central nervous system, with high concentrations found in the basal ganglia, limbic system, and cortex.

Dysfunction of dopamine receptors has been implicated in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder (ADHD), drug addiction, and depression. Therefore, drugs targeting dopamine receptors have been developed for the treatment of these conditions.

Dopamine D2 receptor is a type of metabotropic G protein-coupled receptor that binds to the neurotransmitter dopamine. It is one of five subtypes of dopamine receptors (D1-D5) and is encoded by the gene DRD2. The activation of D2 receptors leads to a decrease in the activity of adenylyl cyclase, which results in reduced levels of cAMP and modulation of ion channels.

D2 receptors are widely distributed throughout the central nervous system (CNS) and play important roles in various physiological functions, including motor control, reward processing, emotion regulation, and cognition. They are also involved in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, drug addiction, and Tourette syndrome.

D2 receptors have two main subtypes: D2 short (D2S) and D2 long (D2L). The D2S subtype is primarily located in the presynaptic terminals and functions as an autoreceptor that regulates dopamine release, while the D2L subtype is mainly found in the postsynaptic neurons and modulates intracellular signaling pathways.

Antipsychotic drugs, which are used to treat schizophrenia and other psychiatric disorders, work by blocking D2 receptors. However, excessive blockade of these receptors can lead to side effects such as extrapyramidal symptoms (EPS), tardive dyskinesia, and hyperprolactinemia. Therefore, the development of drugs that selectively target specific subtypes of dopamine receptors is an active area of research in the field of neuropsychopharmacology.

Dopamine antagonists are a class of drugs that block the action of dopamine, a neurotransmitter in the brain associated with various functions including movement, motivation, and emotion. These drugs work by binding to dopamine receptors and preventing dopamine from attaching to them, which can help to reduce the symptoms of certain medical conditions such as schizophrenia, bipolar disorder, and gastroesophageal reflux disease (GERD).

There are several types of dopamine antagonists, including:

1. Typical antipsychotics: These drugs are primarily used to treat psychosis, including schizophrenia and delusional disorders. Examples include haloperidol, chlorpromazine, and fluphenazine.
2. Atypical antipsychotics: These drugs are also used to treat psychosis but have fewer side effects than typical antipsychotics. They may also be used to treat bipolar disorder and depression. Examples include risperidone, olanzapine, and quetiapine.
3. Antiemetics: These drugs are used to treat nausea and vomiting. Examples include metoclopramide and prochlorperazine.
4. Dopamine agonists: While not technically dopamine antagonists, these drugs work by stimulating dopamine receptors and can be used to treat conditions such as Parkinson's disease. However, they can also have the opposite effect and block dopamine receptors in high doses, making them functionally similar to dopamine antagonists.

Common side effects of dopamine antagonists include sedation, weight gain, and movement disorders such as tardive dyskinesia. It's important to use these drugs under the close supervision of a healthcare provider to monitor for side effects and adjust the dosage as needed.

Chrzanowski FA, McGrogan BA, Maryanoff BE (March 1985). "The pKa of butaclamol and the mode of butaclamol binding to central ... Butaclamol (AY-23,028) is a type of antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...
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Chrzanowski FA, McGrogan BA, Maryanoff BE (March 1985). "The pKa of butaclamol and the mode of butaclamol binding to central ... Butaclamol (AY-23,028) is a type of antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...
... butaclamol 7.2; trifluperidol 6.8; haloperidol 6.7; spiroperidol 6.3; (-)-butaclamol 5.3; clozapine 7.0; and sulpiride 5.7. ...
Another set of slides containing consecutive sections was incubated in the same conditions in the presence of butaclamol (10 μM ...
Phenothiazines or butyrophenones are known to act at both pre and post-synaptic dopamine receptors, whereas butaclamol or ...
... isomers of butaclamol, but dopamine, apomorphine, and chlorpromazine sulfoxide were not inhibitory. Muscarinic agonists ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
A knowledge graph of biological entities such as genes, gene functions, diseases, phenotypes and chemicals. Embeddings are generated with Walking RDF and OWL method ...
Chlorpromazine, thiothixene, (+) butaclamol and cisflupenthixol showed a 3-4-fold discrimination between lines. The specific D1 ... Chlorpromazine, thiothixene, (+) butaclamol and cisflupenthixol showed a 3-4-fold discrimination between lines. The specific D1 ... Chlorpromazine, thiothixene, (+) butaclamol and cisflupenthixol showed a 3-4-fold discrimination between lines. The specific D1 ... Chlorpromazine, thiothixene, (+) butaclamol and cisflupenthixol showed a 3-4-fold discrimination between lines. The specific D1 ...
Butaclamol-like neuroleptic agents: Synthesis of 1-(11H-dibenz[b,f]-1,4-oxathiepin-11-yl)methyl-4-isobutylpiperidin-4-ol and of ...
Butaclamol-like neuroleptic agents: Synthesis of 1-(11H-dibenz[b,f]-1,4-oxathiepin-11-yl)methyl-4-isobutylpiperidin-4-ol and of ...
Conversely, dopaminergic antagonist type-1, butaclamol, attenuated exercise control of serum TNF levels. These results suggest ...
Responses to dopamine were reversibly suppressed by the non-selective antagonist (+)-butaclamol (10−7moll-1). Although the ... butaclamol hydrochloride (Research Biochemicals), cis-(Z)-flupenthixol dihydrochloride (Lundbeck), SCH 23390(7-chloro-8-hydroxy ...
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Tricyclics: Amoxapine • Butaclamol • Fluotracen • Loxapine • Metitepine/Methiothepin • Octoclothiepin • Trimipramine; Others: ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
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butaclamol Hs. Antagonist. 7.5 - 8.7 pKi 25,41,75,125 ...

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