Neuroleptic Malignant Syndrome: 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)Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.Psychotic Disorders: 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)Antipsychotic Agents: 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.Dosage Forms: 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.Inventions: A novel composition, device, or process, independently conceived de novo or derived from a pre-existing model.Schizophrenia: A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.Attention Deficit Disorder with Hyperactivity: 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)Methylphenidate: 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.Learning Disorders: 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.Blood Platelet Disorders: Disorders caused by abnormalities in platelet count or function.Fecal Incontinence: Failure of voluntary control of the anal sphincters, with involuntary passage of feces and flatus.Urinary Incontinence, Stress: 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.Receptors, Dopamine: Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells.Selective Estrogen Receptor Modulators: 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)Dopamine: 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.Receptors, Dopamine D2: 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.Receptors, Dopamine D1: 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.Dopamine Agonists: Drugs that bind to and activate dopamine receptors.Raloxifene: 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.Cyclic AMP: 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.Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 22.214.171.124.Nasal Decongestants: 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)Fraud: Exploitation through misrepresentation of the facts or concealment of the purposes of the exploiter.Counterfeit Drugs: 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.Streptomyces: 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.Chemistry: A basic science concerned with the composition, structure, and properties of matter; and the reactions that occur between substances and the associated energy exchange.Fermentation: 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.Chemical Phenomena: The composition, conformation, and properties of atoms and molecules, and their reaction and interaction processes.Microscopy, Interference: The science and application of a double-beam transmission interference microscope in which the illuminating light beam is split into two paths. One beam passes through the specimen while the other beam reflects off a reference mirror before joining and interfering with the other. The observed optical path difference between the two beams can be measured and used to discriminate minute differences in thickness and refraction of non-stained transparent specimens, such as living cells in culture.Glass: Hard, amorphous, brittle, inorganic, usually transparent, polymerous silicate of basic oxides, usually potassium or sodium. It is used in the form of hard sheets, vessels, tubing, fibers, ceramics, beads, etc.Immersion: The placing of a body or a part thereof into a liquid.HEPES: A dipolar ionic buffer.Electrophysiology: The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.Microtomy: The technique of using a microtome to cut thin or ultrathin sections of tissues embedded in a supporting substance. The microtome is an instrument that hold a steel, glass or diamond knife in clamps at an angle to the blocks of prepared tissues, which it cuts in sections of equal thickness.Microscopy, Phase-Contrast: A form of interference microscopy in which variations of the refracting index in the object are converted into variations of intensity in the image. This is achieved by the action of a phase plate.Research Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Research Support, Non-U.S. Gov'tResearch Support, U.S. GovernmentNeovascularization, Pathologic: A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.Research Support, American Recovery and Reinvestment ActResearch Support, N.I.H., ExtramuralReceptors, Adrenergic, beta-2: 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.beta-Adrenergic Receptor Kinases: G-protein-coupled receptor kinases that mediate agonist-dependent PHOSPHORYLATION and desensitization of BETA-ADRENERGIC RECEPTORS.Arrestins: Regulatory proteins that down-regulate phosphorylated G-protein membrane receptors, including rod and cone photoreceptors and adrenergic receptors.Molecular Sequence Data: 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.Receptors, Adrenergic, beta: 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.Receptors, Adrenergic: 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.Prolactin: A lactogenic hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). It is a polypeptide of approximately 23 kD. Besides its major action on lactation, in some species prolactin exerts effects on reproduction, maternal behavior, fat metabolism, immunomodulation and osmoregulation. Prolactin receptors are present in the mammary gland, hypothalamus, liver, ovary, testis, and prostate.Spiperone: A spiro butyrophenone analog similar to HALOPERIDOL and other related compounds. It has been recommended in the treatment of SCHIZOPHRENIA.Olivopontocerebellar Atrophies: A group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the CEREBELLUM; PONS; and inferior olivary nuclei. Additional clinical features may include MUSCLE RIGIDITY; NYSTAGMUS, PATHOLOGIC; RETINAL DEGENERATION; MUSCLE SPASTICITY; DEMENTIA; URINARY INCONTINENCE; and OPHTHALMOPLEGIA. The familial form has an earlier onset (second decade) and may feature spinal cord atrophy. The sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of MULTIPLE SYSTEM ATROPHY. (From Adams et al., Principles of Neurology, 6th ed, p1085)
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)(+info)
Cuticular plasticization in the tick, Amblyomma hebraeum (Acari: Ixodidae): possible roles of monoamines and cuticular pH. (5/27)(+info)
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)
"The pKa of butaclamol and the mode of butaclamol binding to central dopamine receptors." J. Med. Chem. 28 399-400.. ... Butaclamol (AY-23,028) is a typical antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...
List of dopaminergic drugs
Butaclamol • Ecopipam • N-Ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) • Eticlopride • Fananserin • L-745,870 • ...
Methyl vinyl ketone
... butaclamol, and etretinate. 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 ...
... acepromazine amisulpride amoxapine asenapine azaperone benperidol bromopride butaclamol clomipramine (mild) chlorpromazine ...
List of MeSH codes (D04)
... butaclamol MeSH D04.615.181.384.340 --- cyproheptadine MeSH D04.615.181.384.340.500 --- loratadine MeSH D04.615.181.384.380 ...
List of drugs: Bs-Bz
Butace butaclamol (INN) butadiazamide (INN) butafosfan (INN) Butal compound butalamine (INN) Butalan butalbital (INN) ...
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 ...
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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 - Wikipedia
"The pKa of butaclamol and the mode of butaclamol binding to central dopamine receptors." J. Med. Chem. 28 399-400.. ... Butaclamol (AY-23,028) is a typical antipsychotic which was never marketed. Sold as the hydrochloride salt for use in research ...https://en.wikipedia.org/wiki/Butaclamol
Phenomenex HPLC Application #17397: Butaclamol on Lux Cellulose-1
Butaclamol on Lux Cellulose-1. Column used: Lux® 5 µm Cellulose-1, LC Column 250 x 4.6 mm, Ea Part#: 00G-4459-E0 ...http://www.phenomenex.com/Application/Detail/17397
butaclamol | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY
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.. ...http://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=62
Phenomenex HPLC Application #20211: Butaclamol on Lux 5µm Cellulose-2 in RP
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 ...https://www.phenomenex.com/Application/Detail/20211
Read eBooks online | World Heritage Encyclopedia | Butaclamol
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  Sold as the hydrochloride salt for use in research, the compound acts as a dopamine receptor ...http://worldheritage.org/articles/eng/Butaclamol
Fenoldopam - Wikipedia
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...https://en.wikipedia.org/wiki/Fenoldopam
Captodiame - Wikipedia
Butaclamol. *DR-4485. *EGIS-12233. *Ergolines (e.g., 2-Br-LSD (BOL-148), amesergide, bromocriptine, cabergoline, ...https://en.wikipedia.org/wiki/Captodiame
Patent US6489341 - Methods for the treatment of neuroleptic and related disorders using ... - Google Patents
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.http://www.google.com/patents/US6489341?dq=6,970,917
Patent US6911479 - Methods of treating and preventing pain, anxiety, and incontinence using ... - Google Patents
1 mM (+) butaclamol. Adrenergic. WB 4101. 0.5. 15-30. 50 mM. 30 min. 25 10 mM norepinephrine. ...http://www.google.com/patents/US6911479?dq=6437692
View the content page [c]
Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...http://www.let.rug.nl/~gosse/termpedia2/termpedia.php?language=dutch_general&density=7&link_color=000000&termpedia_system=perl_db&url=http%3A%2F%2Fen.wikipedia.org%2Fwiki%2FNuciferine
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Typical antipsychotics: Butaclamol. *Chlorpromazine. *Chlorprothixene. *Flupentixol (flupenthixol) (+melitracen). *Fluphenazine ...http://www.let.rug.nl/~gosse/termpedia2/termpedia.php?language=dutch_general&density=7&link_color=000000&termpedia_system=perl_db&url=http%3A%2F%2Fen.wikipedia.org%2Fwiki%2FAzapride
List of dopaminergic drugs - Wikipedia
Butaclamol • Ecopipam • N-Ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) • Eticlopride • Fananserin • L-745,870 • ...https://en.wikipedia.org/wiki/List_of_dopaminergic_drugs
Template:Dopamine receptor modulators - wikidoc
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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 ...http://clincancerres.aacrjournals.org/content/17/11/3649
WO1995011894A1 - Histamine h3-receptor antagonists and therapeutic uses thereof - Google Patents
Dopamine 1 Butaclamol 37.30 6.4. Dopamine 2 Spiperone 0.08 3.5. Serotonin 1 Serotonin 4.60 -3.6 ...https://patents.google.com/patent/WO1995011894A1/en
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BUTACLAMOL HCL(cas 55528-08-0) * OCTENIDINE HCl(cas 707-75-5) ...http://www.guidechem.com/cas-121/1218-35-5.html
Noradrenergic and specific serotonergic antidepressant
Butaclamol • EGIS-12,233 • Ketanserin • LY-215,840 • Metitepine/Methiothepin • Pimozide • Ritanserin • SB-258,719 • SB-258,741 ...https://en.academic.ru/dic.nsf/enwiki/649731
Read eBooks online | World Heritage Encyclopedia | Acetophenazine
Butaclamol Fluotracen Loxapine Trimipramine Others Prothipendyl Atypical Benzamides Amisulpride Remoxipride‡ Butyrophenones ...http://worldheritage.org/articles/Acetophenazine
Regulation of Dopamine D1 Receptor Function by Physical Interaction with the NMDA Receptors | Journal of Neuroscience
Nonspecific binding was defined in the presence of 10 μm (+)-butaclamol. Binding data were analyzed by the nonlinear least- ...http://www.jneurosci.org/content/24/5/1149?ijkey=5d5af088766917c6997c24fbabcc5192c0ddf9fd&keytype2=tf_ipsecsha
... butaclamol. Binding data were analyzed with the GraphPad Prism program. Experiments were performed three times in triplicate. ...http://www.jneurosci.org/content/23/15/6245
Biologic effects of dopamine on tumor vasculature in ovarian carcinoma. - PubMed - NCBI
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 ...https://www.ncbi.nlm.nih.gov/pubmed/23633922
Attenuation of intravenous amphetamine reinforcement by central dopamine blockade in rats - Semantic Scholar
DA blockade (pimozide, 0.0625 to 0.5 mg/kg, or (+)-butaclamol, 0.0125 to 0.1 mg/kg) caused periods of increased rate of ... Effect of butaclamol on dopamine-sensitive adenylate cyclase in the rat striatum.. Richard J. Miller, Alan S. Horn, Leslie Lars ... Effect of butaclamol and its enantiomers upon striatal homovanillic acid and adenyl cyclase of olfactory tubercle in rats.. W. ... The behavioral pharmacology of butaclamol hydrochloride (AY-23,028), a new potent neuroleptic drug. Katherine Voith, Francis ...https://www.semanticscholar.org/paper/Attenuation-of-intravenous-amphetamine-by-central-Yokel-Wise/6d54d71b3b110568b24325181cbc9474ead214a9
Nonspecific binding was determined in the presence of 2 μM (+)-butaclamol. Incubations were carried out at 30°C for 60 min and ...http://molpharm.aspetjournals.org/content/61/4/806
Frontiers | Zebrafish as an Animal Model for Drug Discovery in Parkinson's Disease and Other Movement Disorders: A Systematic...
Interestingly, the non-selective dopamine agonist, apomorphine, and dopamine antagonist, butaclamol, induce biphasic dose- ...https://www.frontiersin.org/articles/10.3389/fneur.2018.00347/full
- The pKa of butaclamol and the mode of butaclamol binding to central dopamine receptors. (wikipedia.org)
- Butaclamol ( AY-23,028 ) is an 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)
- 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)