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We examined the involvement of multiple monoaminergic receptors in the induction of spontaneous tail-flicks (STFs) by the open channel blocker at N- methyl-D-aspartate (NMDA) receptors, dizocilpine, and the NMDA recognition site antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP). At doses eliciting a maximal STF response, dizocilpine and CPP elevated levels of norepinephrine, but not dopamine or serotonin, in dialysates of nucleus accumbens, their known locus of action in eliciting STFs. Chemically diverse alpha2-adrenergic receptor (AR) antagonists atipamezole, L745,743, RX821,002, idazoxan, and desfluparoxan abolished induction of STFs by dizocilpine, whereas the preferential alpha1-AR antagonists prazosin, WB4101, and ARC239 were weakly active: relative potencies in blocking STFs correlated significantly with affinity at alpha2-ARs. The D1/D5 receptor antagonists SCH23390, SCH39166, and NNC756 potently abolished STFs, whereas the D2 antagonist L741,626, the D3 antagonists GR218,231 and S14297, and the D4 antagonists S18126 and L745,870 were inactive. D1 and alpha2-AR antagonists also blocked induction of STFs by CPP. Blockade of dizocilpine-induced STFs was specific inasmuch as idazoxan and SCH 23390 did not modify induction of ataxia by dizocilpine. Antagonists at multiple 5-hydroxytryptamine receptors failed to modify induction of STFs. Finally, dizocilpine-induced STFs were blocked by clozapine and 11 other antipsychotics, the potency of which correlated significantly with affinity at alpha2-ARs. In conclusion, STFs evoked by interruption or transmission at NMDA receptors are dependent on D1 receptors and alpha2-ARs for their expression. Antagonism of the alpha2-ARs is involved in their blockade by antipsychotics. This mode should facilitate exploration of interrelationships between glutamatergic and monoaminergic mechanisms involved in psychiatric and neurologic disorders.

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Piperidine – Wikipedia,
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Chemistry is traditionally divided into organic and inorganic chemistry. Computed Properties of C24H25FN4O2. The former is the study of compounds containing at least one carbon-hydrogen bonds.In a patent，Which mentioned a new discovery about 129029-23-8

The present invention relates to the use of low dose pipamperone and compositions comprising the same for the treatment of mood disorders.

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The present invention relates to the use of the compound escitalopram (INN-name), i.e. (S)-1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-5- isobenzofurancarbonitrile, or a pharmaceutically acceptable salt thereof for the preparation of a medicament for improving cognition in a condition where the cognitive processes are diminished.

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Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels.In a patent， Safety of Ocaperidone, Which mentioned a new discovery about 129029-23-8

We have evaluated the proteochemometrics approach in the analysis of the interactions of a diverse set or organic ligands with subtypes of serotonin, dopamine, histamine, and adrenergic receptors. As used herein, proteochemometrics exploits affinity data for series of organic amines binding to wild-type amine G protein-coupled receptors, correlating it to descriptions and cross-description derived from the primary amino acid sequences of the receptors and the computed structures of the organic compounds. We show that after appropriate data preprocessing, statistically valid models that have good external predictive ability can be created. Evaluation of the models gave important quantitative insight into the mode of interactions of the amine G protein-coupled receptors with their ligands.

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The invention provides compositions that include conjugates of a fatty acid molecule, preferably cis-docosahexaenoic acid, and clozapine. The conjugates are useful in treating psychological disorders such as schizophrenia.

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Piperidine – Wikipedia,
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Catalysts function by providing an alternate reaction mechanism that has a lower activation energy than would be found in the absence of the catalyst. In some cases, the catalyzed mechanism may include additional steps.In a article, 129029-23-8, molcular formula is C24H25FN4O2, introducing its new discovery. HPLC of Formula: C24H25FN4O2

The activity of serotonin (5-HT) receptor agonists, partial agonists and antagonists, and various other neurotransmitter receptor antagonists at human 5-HT1(A) receptors that are negatively coupled to adenylate cyclase in permanently transfected HeLa cells was investigated. 5-HT(1A) receptor-mediated inhibition of adenylate cyclase was studied by measuring inhibition of cAMP accumulation, induced by forskolin. At 100 muM forskolin produced a 100-fold increase in cAMP formation: 5-HT concentration dependently inhibited the cAMP formation; maximal inhibition was attained at 1 muM 5-HT and represented 90% of the stimulated cAMP formation. Full inhibition was observed with 5-HT(1A) receptor agonists: N,N-dipropyl-8-hydroxy-2-aminotetralin (8-OH-DPAT) and flesinoxan, and nonselective 5-HT receptor agonists: d-lysergic acid diethylamide (d-LSD), RU 24,969, bufotenine, methysergide and tryptamine. The rank order of potency of the compounds for inhibiting the cAMP formation corresponded to the rank order of the binding affinities of the drugs for the 5-HT(1A) receptor. Partial inhibition was obtained with submicromolar concentrations of buspirone, spiroxatrine and ipsapirone. A slight inhibition was observed with 1 muM 5-HT receptor agonist CP 93129 and 1 muM 5-HT receptor antagonists mesulergine and BW-501. No inhibition was found with: the 5-HT receptor agonists quipazine, sumatriptan and 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM); the 5-HT receptor antagonist ICS-205,930; and other neurotransmitter receptor antagonists such as pindolol, CGP 20712-A, prazosin, sulpiride and pyrilamine. Spiperone and pindolol fully antagonized the agonist-mediated inhibition of forskolin-stimulated cAMP formation. Partial inhibition of the agonist-mediated inhibition of forskolin-stimulated cAMP formation was apparent with 1 muM ocaperidone and 1 muM ipsapirone. It can be concluded that HeLA cells, permanently expressing human 5-HT(1A) receptors, are a valid cellular system for studying the negative coupling of 5-HT(1A) receptors to adenylate cyclase and the action of compounds there upon.

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Inverse agonism at serotonin and cannabinoid receptors

Contemporary receptor theory was developed to account for the existence of constitutive activity, as defined by the presence of receptor signaling in the absence of any ligand. In vitro studies with a variety of cell types have revealed the existence of constitutive activity and inverse agonism at a large number of receptors and also additional complexities of ligandreceptor interactions. Thus, ligands acting at a constitutively active receptor can act as agonists, antagonists, and/or inverse agonists, and these pharmacological characteristics can differ for an individual ligand depending upon the receptor response measured and the physiological state of the system under study. Studies with a variety of cell types have established that the serotonin 5-HT 2A and 5-HT2C receptors and the cannabinoid CB1 receptor demonstrate constitutive activity and inverse agonism in vitro. Serotonin and cannabinoid receptors are involved in a large number of physiological and behavioral functions. The possible existence of constitutive activity and inverse agonism at these receptors in vivo would provide new avenues for drug development. Recent studies have provided compelling evidence that both the serotonin 5-HT2A and 5-HT2C receptors and cannabinoid CB1 receptor demonstrate inverse agonism and constitutive activity also in vivo. This chapter describes our current knowledge of constitutive activity in vitro and then examines the evidence for constitutive activity in vivo.

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[35S]guanosine-5′-O-(3-thio)triphosphate binding as a measure of efficacy at human recombinant dopamine D4.4 receptors: Actions of antiparkinsonian and antipsychotic agents

Recombinant human dopamine D4.4 receptor-mediated G protein activation was characterized in membranes of transfected mammalian (Chinese hamster ovary) cells by the use of [35S]guanosine-5′-O-(3-thio)triphosphate (35S]GTPgammaS) binding. An initial series of experiments defined the conditions (3 muM GDP, 100 mM NaCl, 3 mM MgCl2) under which optimal stimulation (2.2-fold increase in specific [35S]GTPgammaS binding) was achieved with the endogenous agonist dopamine. The number of dopamine- activated G proteins in Chinese hamster ovary-D4.4 membranes was determined through [35S]GTPgammaS isotopic dilution saturation binding, yielding a B(max) value of 2.29 pmol/mg. This compared with a D4.4 receptor B(max) value of 1.40 pmol/mg determined by [3H]spiperone saturation binding, indicating that 1 or 2 G proteins were activated per D4.4 receptor and that there were few or no ‘spare receptors’ in this cell line. Under these conditions, the efficacy for stimulation of [35S]GTPgammaS binding at D4.4 receptors of 12 dopaminergic agonists was determined. Several antiparkinsonian drugs, including ropinirole, quinerolane and lisuride, exhibited agonist activity at D4.4 receptors (E(max) = 74.3%, 72.4% and 32.2%, respectively, compared with dopamine = 100%). The EC50 values for agonist stimulation of [35S]GTPgammaS binding correlated well with the inhibition constants derived from competition binding with [3H]spiperone (r = +.99). However, other antiparkinsonian drugs (bromocriptine, L-DOPA and terguride) showed low affinity and/or were devoid of agonist activity at D4.4 receptors. The potency at D4.4 receptors of the novel, selective D4.4 receptor antagonist L 745,870 was determined, indicating that it has high affinity (K(l) = 1.99 nM) without detectable agonist activity. Furthermore, L 745,870 completely inhibited dopamine-stimulated [35S]GTPgammaS binding with a K(b) value of 1.07 nM. The action of an additional 20 chemically diverse dopaminergic ligands, including clozapine, ziprasidone, sertindole, olanzapine and several other ‘atypical’ antipsychotics, in advanced development was investigated. Each of these ligands shifted the dopamine stimulation curve to the right in a parallel manner consistent with competitive antagonism at this site and yielding K(b) values (32.6, 22.4, 17.2 and 26.5 nM, respectively) that agreed closely with their K(l) values (38.0, 14.9, 18.5 and 26.1 nM). In contrast, raclopride and seroquel exhibited low affinity at D4.4 receptors (K(l) > 1000 nM). Other compounds that showed antagonist activity at D4.4 receptors included the 5- hydroxytryptamine(2A) receptor antagonist fananserin (RP 62203), the sigma ligand BMY 14,802 and the D3 receptor antagonist GR 103,691. In conclusion, dopamine D4.4 receptor activity is unlikely to be an important factor in the clinical effectiveness of antiparkinsonian drugs, although low agonist efficacy at D4.4 receptors might be associated with a lesser incidence of side effects. Furthermore, antagonist activity at D4.4 receptors is a common property of many typical and atypical antipsychotic agents.

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