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.
A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A potentially fatal syndrome associated primarily with the use of neuroleptic agents (see ANTIPSYCHOTIC AGENTS) which are in turn associated with dopaminergic receptor blockade (see RECEPTORS, DOPAMINE) in the BASAL GANGLIA and HYPOTHALAMUS, and sympathetic dysregulation. Clinical features include diffuse MUSCLE RIGIDITY; TREMOR; high FEVER; diaphoresis; labile blood pressure; cognitive dysfunction; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present. (From Adams et al., Principles of Neurology, 6th ed, p1199; Psychiatr Serv 1998 Sep;49(9):1163-72)
Exclusive legal rights or privileges applied to inventions, plants, etc.
Disorders in which there is a loss of ego boundaries or a gross impairment in reality testing with delusions or prominent hallucinations. (From DSM-IV, 1994)
Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.
Completed forms of the pharmaceutical preparation in which prescribed doses of medication are included. They are designed to resist action by gastric fluids, prevent vomiting and nausea, reduce or alleviate the undesirable taste and smells associated with oral administration, achieve a high concentration of drug at target site, or produce a delayed or long-acting drug effect.
A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.
A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.
A behavior disorder originating in childhood in which the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity. Although most individuals have symptoms of both inattention and hyperactivity-impulsivity, one or the other pattern may be predominant. The disorder is more frequent in males than females. Onset is in childhood. Symptoms often attenuate during late adolescence although a minority experience the full complement of symptoms into mid-adulthood. (From DSM-V)
A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.
Conditions characterized by a significant discrepancy between an individual's perceived level of intellect and their ability to acquire new language and other cognitive skills. These disorders may result from organic or psychological conditions. Relatively common subtypes include DYSLEXIA, DYSCALCULIA, and DYSGRAPHIA.
Disorders caused by abnormalities in platelet count or function.
Failure of voluntary control of the anal sphincters, with involuntary passage of feces and flatus.
Involuntary discharge of URINE as a result of physical activities that increase abdominal pressure on the URINARY BLADDER without detrusor contraction or overdistended bladder. The subtypes are classified by the degree of leakage, descent and opening of the bladder neck and URETHRA without bladder contraction, and sphincter deficiency.
A structurally diverse group of compounds distinguished from ESTROGENS by their ability to bind and activate ESTROGEN RECEPTORS but act as either an agonist or antagonist depending on the tissue type and hormonal milieu. They are classified as either first generation because they demonstrate estrogen agonist properties in the ENDOMETRIUM or second generation based on their patterns of tissue specificity. (Horm Res 1997;48:155-63)
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.
Drugs that bind to and activate dopamine receptors.
A second generation selective estrogen receptor modulator (SERM) used to prevent osteoporosis in postmenopausal women. It has estrogen agonist effects on bone and cholesterol metabolism but behaves as a complete estrogen antagonist on mammary gland and uterine tissue.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
Drugs designed to treat inflammation of the nasal passages, generally the result of an infection (more often than not the common cold) or an allergy related condition, e.g., hay fever. The inflammation involves swelling of the mucous membrane that lines the nasal passages and results in inordinate mucus production. The primary class of nasal decongestants are vasoconstrictor agents. (From PharmAssist, The Family Guide to Health and Medicine, 1993)
Exploitation through misrepresentation of the facts or concealment of the purposes of the exploiter.
Drugs manufactured and sold with the intent to misrepresent its origin, authenticity, chemical composition, and or efficacy. Counterfeit drugs may contain inappropriate quantities of ingredients not listed on the label or package. In order to further deceive the consumer, the packaging, container, or labeling, may be inaccurate, incorrect, or fake.
A genus of bacteria that form a nonfragmented aerial mycelium. Many species have been identified with some being pathogenic. This genus is responsible for producing a majority of the ANTI-BACTERIAL AGENTS of practical value.
A basic science concerned with the composition, structure, and properties of matter; and the reactions that occur between substances and the associated energy exchange.
Anaerobic degradation of GLUCOSE or other organic nutrients to gain energy in the form of ATP. End products vary depending on organisms, substrates, and enzymatic pathways. Common fermentation products include ETHANOL and LACTIC ACID.
The composition, conformation, and properties of atoms and molecules, and their reaction and interaction processes.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
G-protein-coupled receptor kinases that mediate agonist-dependent PHOSPHORYLATION and desensitization of BETA-ADRENERGIC RECEPTORS.
Regulatory proteins that down-regulate phosphorylated G-protein membrane receptors, including rod and cone photoreceptors and adrenergic receptors.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.

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)

Post-transcriptional protein synthesis by GH3 cloned pituitary cells, which secrete prolactin and growth hormone, is dependent on Ca2+. The effects of antagonists of prolactin secretion were examined on overall protein synthesis in GH3 cells as a function of cellular Ca2+ depletion and restoration at varying concentrations of extracellular Ca2+. Leucine incorporation by Ca2+-depleted cells during short incubations was reduced by 80-90%. Trifluoperazine at micromolar concentrations inhibited leucine incorporation in a Ca2+-dependent manner. The extent of inhibition varied with extracellular Ca2+ concentration and was fully reversed at higher Ca2+ concentrations. Similar patterns of inhibition of leucine incorporation were observed with nifedipine, verapamil, calmidazolium, chlorpromazine, bromocriptine, ergotamine, and the (+)- and (-)-isomers of butaclamol, but dopamine, apomorphine, and chlorpromazine sulfoxide were not inhibitory. Muscarinic agonists decreased incorporation in a Ca2+-dependent ...
3H]Spiperone, a neuroleptic/dopamine receptor ligand, binds with high affinity (Kd 0.15 nM) to a single specific site on rat corpus striatum membranes. The specific binding represents about 80% of the total binding and is displaced by dopamime, apomorphine, and stereospecifically by neuroleptics such as butaclamol and flupenthixol. However, in contrast to the striatum, only 30-40% of the binding of [3H]spiperone to limbic forebrain membranes is displaced stereospecifically by butaclamol or flupenthixol, whereas dopamine and certain spiperone analogues compete with high affinity for about 70% of the labeled sites. These additional sites are saturable, reversible, and of high affinity. Kinetic analysis of association and dissociation rates yields a Kd value (1.5 nM) in agreement with equilibrium saturation data for these sites. They also possess a precise distribution, with high amounts being found in the hippocampus, septum, and nucleus accumbens, but they are completely absent in areas such as ...
TY - JOUR. T1 - Combination of internal and external plasticization of hydroxypropylated birch xylan tailors the properties of sustainable barrier films. AU - Mikkonen, Kirsi S.. AU - Laine, Christiane. AU - Kontro, Inkeri. AU - Talja, Riku A.. AU - Serimaa, Ritva. AU - Tenkanen, Maija. N1 - Project code: 76880 PY - 2015. Y1 - 2015. N2 - To develop functional and sustainable products from future wood biorefineries, birch kraft pulp xylan was alkali-extracted and modified in aqueous solvent with hydroxypropylation to enhance its processability to films. For the first time, the roles of internal vs. external plasticization in the mechanical, thermal, and barrier performance of xylan films were systematically evaluated as a function of the degree of substitution (DS) of hydroxypropyl (HP) groups (internal plasticizer) and the added sorbitol (external plasticizer). In addition, the moisture uptake and the degree of crystallinity of hydroxypropyl xylan (HPX) films were characterized. Internal ...
Product introduction Coloress transparent oily liruid, boiling point: 170℃(133.3Pa), flash point (open):185℃.Soluble in most organic solvents.small volatility, good compatibility with resin, good plasticization effect. Resistance to coldness,...
The goal of this project is to elucidate the effect of pendant rings and crosslinking on membrane gas separation properties, and design advanced materials with superior gas permeability and selectivity, and great stability against aging and plasticization for practical separations. ...
Hi all, I am hopeing someone out there will be able to help with this question. If you make starch film with glycerol as a softner when does plasticization and antiplasticization happen and what are the differences between them? Thanks in advance. -- Yours Tim ************************************************************************** ____________ \ ______// Tim Eades - tim.eades at F-Secure.com \ \\____ F-Secure Quality Engineering Team \ __// F-Secure Corporation, PL 24, FIN-02231 Espoo, Finland \ \\ tel: +358 9 859 900, direct: +358 9 8599 0105 \ // fax: +358 9 8599 0599 gsm: +358 40 7435049 \/ web: http://www.F-Secure.com/ ...
Buy Renapril (enalapril) 10mg, 5mg online without prescription in USA, Canada, Australia, UK and Europe. Fast order delivery. Worldwide shipping. FDA approved RX online pharmacy.
A notable feature of the PRC of C57BL/6J Per1−/− mice is its high amplitude, which is reminiscent of the light responsiveness of Clock mutant (Δ19) heterozygous mice that have large phase shifts and low-amplitude circadian oscillations in the SCN (Vitaterna et al., 2006). This is consistent with our finding that the Per1−/− SCN is arrhythmic or has a low amplitude, irregular rhythm in vitro (Pendergast et al., 2009). The PRC of Per2−/− mice has an elongated advance zone and large phase advances. In addition, Per2−/− mice have a phase-advanced PRC, suggesting that the phase relationship between the circadian pacemaker and the onset of the activity rhythm in Per2−/− mice is altered. The PRC of Per3−/− mice is similar to the PRC of wild-type mice. This is not surprising because Per3 expression is not induced in response to light (Takumi et al., 1998; Zylka et al., 1998).. PRCs have been used to make predictions according to the discrete model of entrainment, which posits ...
Butaclamol • Ecopipam • N-Ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) • Eticlopride • Fananserin • L-745,870 • ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
Butaclamol. *DR-4485. *EGIS-12233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
... butaclamol, and etretinate.[citation needed] MVK is extremely hazardous upon inhalation causing coughing, wheezing and ...
... butaclamol, ecopipam Tetrahydrobenzazepine: SKF-83959, SKF-82958, SKF-81297, SKF 38393, fenoldopam, 6-Br-APB, SCH 23390 ...
Butace butaclamol (INN) butadiazamide (INN) butafosfan (INN) Butal compound butalamine (INN) Butalan butalbital (INN) ...
... butaclamol MeSH D04.615.181.384.340 - cyproheptadine MeSH D04.615.181.384.340.500 - loratadine MeSH D04.615.181.384.380 - ...
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 typical antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...
... is a member of the sodium channel blocking class of antiepileptic drugs.[60] This may suppress the release of glutamate and aspartate, two of the dominant excitatory neurotransmitters in the CNS.[61] It is generally accepted to be a member of the sodium channel blocking class of antiepileptic drugs,[62] but it could have additional actions since it has a broader spectrum of action than other sodium channel antiepileptic drugs such as phenytoin and is effective in the treatment of the depressed phase of bipolar disorder, whereas other sodium channel blocking antiepileptic drugs are not, possibly on account of its sigma receptor activity. In addition, lamotrigine shares few side-effects with other, unrelated anticonvulsants known to inhibit sodium channels, which further emphasises its unique properties.[63] It is a triazine derivate that inhibits voltage-sensitive sodium channels, leading to stabilization of neuronal membranes. It also blocks L-, N-, and P-type calcium channels and ...
... binds and reversibly inactivates the cholinesterases, thus inhibiting hydrolysis of acetylcholine. This increases acetylcholine concentrations at cholinergic synapses.[1] The precise mechanism of action of donepezil in patients with Alzheimer's disease is not fully understood. Certainly, Alzheimer's disease involves a substantial loss of the elements of the cholinergic system and it is generally accepted that the symptoms of Alzheimer's disease are related to this cholinergic deficit, particularly in the cerebral cortex and other areas of the brain.[18][19] It is noted that the hippocampal formation plays an important role in the processes of control of attention, memory and learning. Just the severity of the loss of cholinergic neurons of the central nervous system (CNS) has been found to correlate with the severity of cognitive impairment. In addition to its actions as an acetylcholinesterase inhibitor, donepezil has been found to act as a potent agonist of the σ1 receptor (Ki = ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
... (CBZ), sold under the trade name Tegretol among others, is an anticonvulsant medication used primarily in the treatment of epilepsy and neuropathic pain.[1] It is not effective for absence or myoclonic seizures.[1] It is used in schizophrenia along with other medications and as a second-line agent in bipolar disorder.[3][1] Carbamazepine appears to work as well as phenytoin and valproate for focal and generalised seizures.[4] Common side effects include nausea and drowsiness.[1] Serious side effects may include skin rashes, decreased bone marrow function, suicidal thoughts, or confusion.[1] It should not be used in those with a history of bone marrow problems.[1] Use during pregnancy may cause harm to the baby; however, stopping the medication in pregnant women with seizures is not recommended.[1] Its use during breastfeeding is not recommended.[1] Care should be taken in those with either kidney or liver problems.[1] Carbamazepine was discovered in 1953 by Swiss chemist Walter ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
... is a molecule which binds to sigma receptors.[1] 4-PPBP decreases neuronal nitric oxide synthase (nNOS) activity and ischemia-evoked nitric oxide (NO) production. 4-PPBP provides neuroprotection; this involves the prevention of ischemia-induced intracellular Ca2+dysregulation.[2]4-PPBP protects neurons using a mechanism that activates the transcription factor cyclic adenosine monophosphate response element-binding protein (CREB). Neuroprotection that is associated with 4-PPBP increases Bcl-2 expression; Bcl-2 expression is regulated by CREB. [3] ...
... is an allosteric endocannabinoid, as it is a negative allosteric modulator of the CB1 receptor.[4][5] Pregnenolone is involved in a natural negative feedback loop against CB1 receptor activation in animals.[6][better source needed] It prevents CB1 receptor agonists like tetrahydrocannabinol, the main active constituent in cannabis, from fully activating the CB1 [6][better source needed] Pregnenolone has been found to bind with high, nanomolar affinity to microtubule-associated protein 2 (MAP2) in the brain.[7][8] In contrast to pregnenolone, pregnenolone sulfate did not bind to microtubules.[7][8] However, progesterone did and with similar affinity to pregnenolone, although unlike pregnenolone, it did not increase binding of MAP2 to tubulin.[7][8] Pregnenolone was found to induce tubule polymerization in neuronal cultures and to increase neurite growth in PC12 cells treated with nerve growth factor.[7][8] As such, pregnenolone may control formation and stabilization of microtubules ...
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 typical antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...
Butaclamol on Lux Cellulose-1. Column used: Lux® 5 µm Cellulose-1, LC Column 250 x 4.6 mm, Ea Part#: 00G-4459-E0 ...
butaclamol ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... One of the two enantiomers found in the INN-assigned racemic compound butaclamol.. ...
Butaclamol on Lux 5µm Cellulose-2 in RP. Column used: Lux® 5 µm Cellulose-2, LC Column 250 x 4.6 mm, Ea Part#: 00G-4457-E0 ...
F. A. Chrzanowski, B. A. McGrogan, B. E. Maryanoff (1985). "The pKa of butaclamol and the mode of butaclamol binding to central ... Butaclamol (AY-23,028) is an [1] Sold as the hydrochloride salt for use in research, the compound acts as a dopamine receptor ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Butaclamol. *DR-4485. *EGIS-12,233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...
The invention relates to methods of administering pharmaceutical compositions and dosage forms comprising the sertindole derivatives nor-sertindole, 5-oxo-sertindole, dehydro-sertindole, and dehydro-nor-sertindol. The methods of the invention are directed to the treatment and prevention of neuroleptic and related disorders such as, psychotic disorders, depression, anxiety, substance addiction, memory impairment and pain.
Butaclamol • Ecopipam • N-Ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) • Eticlopride • Fananserin • L-745,870 • ...
1 mM (+) butaclamol. Adrenergic. WB 4101. 0.5. 15-30. 50 mM. 30 min. 25 10 mM norepinephrine. ...
Butaclamol. 66.7 ± 4.5 (6). 73.8 ± 7.9 (8). D2/D1-like Phentolamine. 71.6 ± 7.1 (6). 64.6 ± 14.9 (10). α-Adrenergic. ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Butaclamol / pharmacology * Male * Nerve Endings / metabolism* * Olfactory Bulb / metabolism* * Olfactory Nerve / metabolism* ...
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...
Nonspecific binding was defined in the presence of 10 μm (+)-butaclamol. Binding data were analyzed by the nonlinear least- ...
Nonspecific binding was determined with 2 μM (+)-butaclamol. KDand Bmax values were determined by fitting data to a one-site ... In contrast, the antagonists butaclamol and haloperidol bound with higher affinity to the noncoupled state. Consistent with the ... Butaclamol and haloperidol, D2 receptor antagonists, bound with slightly higher affinity to the antagonist-labeled noncoupled ... butaclamol hydrochloride, S(−)-PPP, terguride, quinpirole hydrochloride, Tris, EDTA, BSA, and polyethylenimine were purchased ...
Agonist (DR1, SKF 38393; DR2, bromocriptine) and antagonist (DR1, butaclamol; DR2, eticlopride) were used at 50 μmol/L, ... whereas butaclamol, a DR1-specific antagonist, did not affect cell invasion. B, DA blocked the stimulatory effect of NE alone ( ... butaclamol (DR1 antagonist), and norepinephrine (NE) were obtained from Sigma Aldrich; recombinant human VEGF was from R&D ...
This DA stimulatory effect was reversed by DA + butaclamol treatment (†P , .05). In contrast, DA + eticlopride induced a ... DA and the DR1 agonist SKF38393 significantly stimulated 10T1/2 cell migration (*P , .05 compared with NT cells); butaclamol, a ... butaclamol significantly reversed the stimulatory effect of DA on pericyte coverage (†P , .01). (C) Representative images (200x ... butaclamol, or DA + eticlopride. DA significantly blocked tumor growth and reduced the number of tumor nodules in stressed mice ...
Dopamine 1 Butaclamol 37.30 6.4. Dopamine 2 Spiperone 0.08 3.5. Serotonin 1 Serotonin 4.60 -3.6 ...
BUTACLAMOL HCL(cas 55528-08-0) * OCTENIDINE HCl(cas 707-75-5) ...
Butaclamol. Klassifikation: Verschiedene Klassifikationen versuchen morphologische oder pathophysiologische Umstände ...
Third, we identified several dopamine D2 receptor antagonists (triflupromazine, butaclamol, clozapine) that caused a phase ...
... and butaclamol; Fig. 4 C and D and Table S1). Finally, our screen was completed in 25 experimental days, which included ...
Non-specific binding was defined as the binding in the presence of 10 μM (+)-butaclamol. The binding values (n = 3, in ... Non-specific binding was defined by radioligand binding in the presence of 10 μM (+) butaclamol (Sigma-Aldrich, Sweden). The ... butaclamol. The binding values (n = 4, in triplicate) are given in percent of specific binding at the lowest concentration of ...
Interestingly, the non-selective dopamine agonist, apomorphine, and dopamine antagonist, butaclamol, induce biphasic dose- ...
Abdominal vagotomy and intraperitoneal administration of butaclamol (but not spiperone) inhibited the effects of EA. ... for 30 min and then received EA for 30 min with or without abdominal vagotomy or intraperitoneal administration of butaclamol ( ...
Nonspecific binding was determined in the presence of 2 μM (+)-butaclamol. Incubations were carried out at 30°C for 60 min and ...
Butaclamol • EGIS-12,233 • Ketanserin • LY-215,840 • Metitepine/Methiothepin • Pimozide • Ritanserin • SB-258,719 • SB-258,741 ...
Pulsatile growth hormone and prolactin: effects of (+) butaclamol, a dopamine receptor blocking agent. Willoughby, J.O., ... butaclamol, in 10 male rats chronically implanted with right atrial cannulae [42]. ...
Another set of slides containing consecutive sections was incubated in the same conditions in the presence of butaclamol (10 μM ...
  • Rats were subjected to gut ischaemia for 30 min and then received EA for 30 min with or without abdominal vagotomy or intraperitoneal administration of butaclamol (D1 receptor antagonist) or spiperone (D2 receptor antagonist). (greenmedinfo.com)
  • Abdominal vagotomy and intraperitoneal administration of butaclamol (but not spiperone) inhibited the effects of EA. (greenmedinfo.com)
  • The pharmacological profile of binding in cortex was also similar to striatum (epidepride greater than spiperone greater than butaclamol = flupenthixol greater than clozapine) except that an additional low-affinity site, blocked by the alpha-2 adrenergic antagonist idazoxan, was present in cortex. (nih.gov)
  • However, in contrast to the striatum, only 30-40% of the binding of [ 3 H]spiperone to limbic forebrain membranes is displaced stereospecifically by butaclamol or flupenthixol, whereas dopamine and certain spiperone analogues compete with high affinity for about 70% of the labeled sites. (aspetjournals.org)
  • Antagonism of dopamine-induced inhibition of VIP-enhanced cAMP levels by spiperone, (+)-butaclamol, (-)-sulpiride, and SCH23390 occurred at concentrations expected from K 1 values for these antagonists at the D 2 -receptor and was stereoselective. (elsevier.com)
  • Specific binding of D2R to [3H]spiperone was verified by Scatchard plot with (+) butaclamol as a specific inhibitor. (bvsalud.org)
  • Butaclamol ( AY-23,028 ) is an [1] Sold as the hydrochloride salt for use in research, the compound acts as a dopamine receptor antagonist. (worldheritage.org)
  • Effect of butaclamol on dopamine-sensitive adenylate cyclase in the rat striatum. (semanticscholar.org)
  • In the swabbing studies, the pharmacological and kinetic properties of butaclamol-displaceable binding were investigated, and the following results suggest that [ 3H ]spiroperidol binds specifically to only a single site within the basal forebrain of tissue sections and that the site is the dopamine D-2 receptor. (elsevier.com)
  • 2) Dopamine antagonists, such asd haloperidol and butaclamol, were much more effective than dopamine agonists or the serotonin S-2 ligand, ketanserin, in inhibiting [ 3 H]spiroperidol binding. (elsevier.com)
  • Butaclamol elicited a similar stimulation of forskolin-stimulated cyclic AMP accumulation in a CHO cell line expressing human D-2long dopamine receptors whereas it exhibited no stimulating effect on forskolin-stimulated cyclic AMP accumulation in untransfected CHO-K1 cells. (kent.ac.uk)
  • 4 The effects of both (+)-butaclamol and dopamine in CHO-D2S cells were inhibited by pre-treatment with pertussis toxin indicating a role for Gi/Go proteins. (kent.ac.uk)
  • 5 UH232 did not significantly affect forskolin-stimulated cyclic AMP accumulation but this substance was able to inhibit the effects of both dopamine and (+)-butaclamol in a concentration-dependent manner. (kent.ac.uk)
  • However, all of the antagonists tested, apart from UH232 and (-)-butaclamol, were able to increase cyclic AMP accumulation above the forskolin control level. (kent.ac.uk)
  • Domperidone or (+)-butaclamol displaced [3H] spiroperidol from the anterior caudate-putamen, nucleus accumbens, olfactory tubercle, claustrum, layer 5A of motor cortex and layer 1 of the anterior cingulate cortex (IC50 = 2-80 nM). (aspetjournals.org)
  • 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 D 2 and/or D 4 receptors (clozapine, haloperidol, (±)-sulpiride, domperidone, clozapine, risperidone, chlorpromazine, (+)-butaclamol and L-741,742). (biomedcentral.com)
  • The "specific" binding represents about 80% of the total binding and is displaced by dopamime, apomorphine, and stereospecifically by neuroleptics such as butaclamol and flupenthixol. (aspetjournals.org)
  • Intrastriatal injection of kainic acid substantially reduced 1 μM (+)-butaclamol-displaceable binding, indicating that the receptors are in large part on intrinsic striatal neurons. (elsevier.com)
  • One of the two enantiomers found in the INN-assigned racemic compound butaclamol. (guidetopharmacology.org)
  • Effect of butaclamol and its enantiomers upon striatal homovanillic acid and adenyl cyclase of olfactory tubercle in rats. (semanticscholar.org)
  • By using 3 H-spiroperidol as a ligand, saturability (in the amolar range), stereospecificity (by using butaclamol- or thioxanthene-isomers), tissue linearity, and pH- or temperature-dependence were all demonstrated. (edu.sa)
  • The [3H]spiroperidol binding displaced by (+)-butaclamol was resolved into a dopaminergic (D2) component, displaced by 100 microM 2-amino-6,7-dihydroxytetrahydronapthalene or 10 microM (-)-sulpiride and a serotonergic (S2) component, displaced by 40 nM ketanserin or 100 nM methysergide. (aspetjournals.org)
  • Butaclamol (AY-23,028) is a typical antipsychotic which was never marketed. (wikipedia.org)
  • Thus the effects of (+)-butaclamol on forskolin-stimulated cyclic AMP accumulation an mediated directly via the D-2 receptor rather than by reversal of the effects of an endogenous agonist. (kent.ac.uk)
  • A and B) Tumor weight and tumor nodules in nonstressed and stressed mice bearing SKOV3ip1 and HeyA8 tumors treated with PBS (control), DA, DA + butaclamol, or DA + eticlopride. (nih.gov)