The Behavioral and Neurochemical Effects of a Novel d-Amino Acid Oxidase Inhibitor Compound 8 [4 H-Thieno [3,2-b]pyrrole-5-carboxylic Acid] and d-Serine
Multiple studies indicate that N-methyl-d-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for improving NMDA receptor function is to enhance occupancy of the glycine modulatory site on the NMDA receptor by increasing the availability...
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Published in | The Journal of pharmacology and experimental therapeutics Vol. 328; no. 3; pp. 921 - 930 |
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Main Authors | , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.03.2009
American Society for Pharmacology and Experimental Therapeutics |
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Abstract | Multiple studies indicate that N-methyl-d-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for improving NMDA receptor function is to enhance occupancy of the glycine modulatory site on the NMDA receptor by increasing the availability of the endogenous coagonists d-serine. Here, we characterized a novel d-amino acid oxidase (DAAO) inhibitor, compound 8 [4 H-thieno [3,2-b]pyrrole-5-carboxylic acid] and compared it with d-serine. Compound 8 is a moderately potent inhibitor of human (IC50, 145 nM) and rat (IC50, 114 nM) DAAO in vitro. In rats, compound 8 (200 mg/kg) decreased kidney DAAO activity by ∼96% and brain DAAO activity by ∼80%. This marked decrease in DAAO activity resulted in a significant (p < 0.001) elevation in both plasma (220% of control) and cerebrospinal fluid (CSF; 175% of control) d-serine concentration. However, compound 8 failed to significantly influence amphetamine-induced psychomotor activity, nucleus accumbens dopamine release, or an MK-801 (dizocilpine maleate)-induced deficit in novel object recognition in rats. In contrast, high doses of d-serine attenuated both amphetamine-induced psychomotor activity and dopamine release and also improved performance in novel object recognition. Behaviorally efficacious doses of d-serine (1280 mg/kg) increased CSF levels of d-serine 40-fold above that achieved by the maximal dose of compound 8. These findings demonstrate that pharmacological inhibition of DAAO significantly increases d-serine concentration in the periphery and central nervous system. However, acute inhibition of DAAO appears not to be sufficient to increase d-serine to concentrations required to produce antipsychotic and cognitive enhancing effects similar to those observed after administration of high doses of exogenous d-serine. |
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AbstractList | Multiple studies indicate that N -methyl- d -aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for improving
NMDA receptor function is to enhance occupancy of the glycine modulatory site on the NMDA receptor by increasing the availability
of the endogenous coagonists d -serine. Here, we characterized a novel d -amino acid oxidase (DAAO) inhibitor, compound 8 [4 H -thieno [3,2- b ]pyrrole-5-carboxylic acid] and compared it with d -serine. Compound 8 is a moderately potent inhibitor of human (IC 50 , 145 nM) and rat (IC 50 , 114 nM) DAAO in vitro. In rats, compound 8 (200 mg/kg) decreased kidney DAAO activity by â¼96% and brain DAAO activity by
â¼80%. This marked decrease in DAAO activity resulted in a significant ( p < 0.001) elevation in both plasma (220% of control) and cerebrospinal fluid (CSF; 175% of control) d -serine concentration. However, compound 8 failed to significantly influence amphetamine-induced psychomotor activity, nucleus
accumbens dopamine release, or an MK-801 (dizocilpine maleate)-induced deficit in novel object recognition in rats. In contrast,
high doses of d -serine attenuated both amphetamine-induced psychomotor activity and dopamine release and also improved performance in novel
object recognition. Behaviorally efficacious doses of d -serine (1280 mg/kg) increased CSF levels of d -serine 40-fold above that achieved by the maximal dose of compound 8. These findings demonstrate that pharmacological inhibition
of DAAO significantly increases d -serine concentration in the periphery and central nervous system. However, acute inhibition of DAAO appears not to be sufficient
to increase d -serine to concentrations required to produce antipsychotic and cognitive enhancing effects similar to those observed after
administration of high doses of exogenous d -serine. Multiple studies indicate that N-methyl-d-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for improving NMDA receptor function is to enhance occupancy of the glycine modulatory site on the NMDA receptor by increasing the availability of the endogenous coagonists d-serine. Here, we characterized a novel d-amino acid oxidase (DAAO) inhibitor, compound 8 [4 H-thieno [3,2-b]pyrrole-5-carboxylic acid] and compared it with d-serine. Compound 8 is a moderately potent inhibitor of human (IC50, 145 nM) and rat (IC50, 114 nM) DAAO in vitro. In rats, compound 8 (200 mg/kg) decreased kidney DAAO activity by ∼96% and brain DAAO activity by ∼80%. This marked decrease in DAAO activity resulted in a significant (p < 0.001) elevation in both plasma (220% of control) and cerebrospinal fluid (CSF; 175% of control) d-serine concentration. However, compound 8 failed to significantly influence amphetamine-induced psychomotor activity, nucleus accumbens dopamine release, or an MK-801 (dizocilpine maleate)-induced deficit in novel object recognition in rats. In contrast, high doses of d-serine attenuated both amphetamine-induced psychomotor activity and dopamine release and also improved performance in novel object recognition. Behaviorally efficacious doses of d-serine (1280 mg/kg) increased CSF levels of d-serine 40-fold above that achieved by the maximal dose of compound 8. These findings demonstrate that pharmacological inhibition of DAAO significantly increases d-serine concentration in the periphery and central nervous system. However, acute inhibition of DAAO appears not to be sufficient to increase d-serine to concentrations required to produce antipsychotic and cognitive enhancing effects similar to those observed after administration of high doses of exogenous d-serine. Multiple studies indicate that N-methyl-D-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for improving NMDA receptor function is to enhance occupancy of the glycine modulatory site on the NMDA receptor by increasing the availability of the endogenous coagonists D-serine. Here, we characterized a novel D-amino acid oxidase (DAAO) inhibitor, compound 8 [4H-thieno [3,2-b]pyrrole-5-carboxylic acid] and compared it with D-serine. Compound 8 is a moderately potent inhibitor of human (IC(50), 145 nM) and rat (IC(50), 114 nM) DAAO in vitro. In rats, compound 8 (200 mg/kg) decreased kidney DAAO activity by approximately 96% and brain DAAO activity by approximately 80%. This marked decrease in DAAO activity resulted in a significant (p < 0.001) elevation in both plasma (220% of control) and cerebrospinal fluid (CSF; 175% of control) D-serine concentration. However, compound 8 failed to significantly influence amphetamine-induced psychomotor activity, nucleus accumbens dopamine release, or an MK-801 (dizocilpine maleate)-induced deficit in novel object recognition in rats. In contrast, high doses of D-serine attenuated both amphetamine-induced psychomotor activity and dopamine release and also improved performance in novel object recognition. Behaviorally efficacious doses of D-serine (1280 mg/kg) increased CSF levels of D-serine 40-fold above that achieved by the maximal dose of compound 8. These findings demonstrate that pharmacological inhibition of DAAO significantly increases D-serine concentration in the periphery and central nervous system. However, acute inhibition of DAAO appears not to be sufficient to increase D-serine to concentrations required to produce antipsychotic and cognitive enhancing effects similar to those observed after administration of high doses of exogenous D-serine. |
Author | Sparey, Tim Mullins, Chadwick M. Hinchliffe, Richard M. Jones, Brian McNaughton, Caitlyn H. Uslaner, Jason M. Pascarella, Danette M. Jacobson, Marlene A. Yao, Lihang Venkatraman, Shankar Brandon, Nicholas J. Surles, Nathan O. Huszar, Sarah L. Hutson, Peter H. Young, Mary Beth Kandebo, Monika Sachs, Nancy Smith, Sean M. |
Author_xml | – sequence: 1 givenname: Sean M. surname: Smith fullname: Smith, Sean M. email: sean_smith2@merck.com – sequence: 2 givenname: Jason M. surname: Uslaner fullname: Uslaner, Jason M. – sequence: 3 givenname: Lihang surname: Yao fullname: Yao, Lihang – sequence: 4 givenname: Chadwick M. surname: Mullins fullname: Mullins, Chadwick M. – sequence: 5 givenname: Nathan O. surname: Surles fullname: Surles, Nathan O. – sequence: 6 givenname: Sarah L. surname: Huszar fullname: Huszar, Sarah L. – sequence: 7 givenname: Caitlyn H. surname: McNaughton fullname: McNaughton, Caitlyn H. – sequence: 8 givenname: Danette M. surname: Pascarella fullname: Pascarella, Danette M. – sequence: 9 givenname: Monika surname: Kandebo fullname: Kandebo, Monika – sequence: 10 givenname: Richard M. surname: Hinchliffe fullname: Hinchliffe, Richard M. – sequence: 11 givenname: Tim surname: Sparey fullname: Sparey, Tim – sequence: 12 givenname: Nicholas J. surname: Brandon fullname: Brandon, Nicholas J. – sequence: 13 givenname: Brian surname: Jones fullname: Jones, Brian – sequence: 14 givenname: Shankar surname: Venkatraman fullname: Venkatraman, Shankar – sequence: 15 givenname: Mary Beth surname: Young fullname: Young, Mary Beth – sequence: 16 givenname: Nancy surname: Sachs fullname: Sachs, Nancy – sequence: 17 givenname: Marlene A. surname: Jacobson fullname: Jacobson, Marlene A. – sequence: 18 givenname: Peter H. surname: Hutson fullname: Hutson, Peter H. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19088300$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1016/j.mcn.2006.05.003 10.1523/JNEUROSCI.23-20-07586.2003 10.1177/1087057106288181 10.1016/j.pnpbp.2005.04.023 10.1517/14728214.10.4.827 10.1016/S0006-3223(98)00279-0 10.1038/sj.npp.1300772 10.1016/0896-6273(92)90207-T 10.1001/archpsyc.60.6.572 10.1038/sj.mp.4001421 10.1016/j.biopsych.2003.09.012 10.1111/j.1460-9568.2007.05769.x 10.1016/0165-6147(93)90108-V 10.1093/genetics/103.2.277 10.1016/j.pnpbp.2003.09.004 10.1073/pnas.182412499 10.1016/j.biopsych.2007.04.038 10.1016/j.neures.2005.05.008 10.1001/archpsyc.56.1.29 10.1016/S0026-895X(25)09633-6 10.1016/j.bmcl.2008.04.020 10.1016/S0021-9258(19)74201-X 10.1192/bjp.169.5.610 10.1016/S0006-8993(02)03466-2 10.1016/S0378-4347(01)00131-1 10.1016/0304-3940(93)90476-2 10.1016/S0893-133X(01)00243-3 10.1073/pnas.97.9.4926 10.1016/S0896-6273(03)00757-8 10.1001/archpsyc.1994.03950030035004 10.1111/j.1460-9568.2007.05446.x 10.1093/cercor/bhh147 10.1016/0020-711X(92)90322-R 10.1176/appi.ajp.159.3.480 10.1016/j.biopsych.2005.06.032 10.1016/j.euroneuro.2007.06.006 10.1016/0378-4347(92)80300-F 10.1038/325529a0 10.1152/ajprenal.00441.2006 |
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References | 519-524. Tsai G, Lane HY, Yang P, Chong MY, and Lange N (2004) Glycine transporter I inhibitor Hashimoto A, Nishikawa T, Konno R, Niwa A, Oka T, and Takahashi K (1993) Free 13675-13680. 34-38. aspartate oxidase: effects of 26941-26949. 199-214. 1081-1090. 12-35. 203-207. Konno R and Yasumura Y (1983) Mouse mutant deficient in methyl- aspartic acid 7th ed. Institute of Laboratory Animal Resources, Commission on Life Sciences, National Research Council, Washington, DC. Schumacher J, Jamra RA, Freudenberg J, Becker T, Ohlraun S, Otte AC, Tullius M, Kovalenko S, Bogaert AV, Maier W, et al. (2004) Examination of G72 and methylglycine (sarcosine), added to antipsychotics for the treatment of schizophrenia. Kinney GG, Sur C, Burno M, Mallorga PJ, Williams JB, Figueroa DJ, Wittmann M, Lemaire W, and Conn PJ (2003) The glycine transporter type 1 inhibitor 230-234. amino acid oxidase. 29-36. Alanine added to antipsychotics for the treatment of schizophrenia. Amino acid oxidase and serine racemase in human brain: normal distribution and altered expression in schizophrenia. Adage T, Trillat AC, Quattropani A, Perrin D, Cavarec L, Shaw J, Guerassimenko O, Giachetti C, Gréco B, Chumakov I, et al. (2008) In vitro and in vivo pharmacological profile of AS057278, a selective Javitt DC (1987) Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia. serine and serine reuptake in the mouse CNS. Amino-acid oxidase and its physiological function. amino acid oxidase and Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, and Tamminga CA (2001) Effects of ketamine in normal and schizophrenic volunteers. aminoacid oxidase as genetic risk factors for schizophrenia and bipolar affective disorder. 20-25. amino acid oxidase (DAO) inhibitors. 452-456. Krug AW, Völker K, Dantzler WH, and Silbernagl S (2007) Why is McBain CJ, Kleckner NW, Wyrick S, and Dingledine R (1989) Structural requirements for activation of the glycine coagonist site of aspartate receptors expressed in Xenopus oocytes. Maekawa M, Watanabe M, Yamaguchi S, Konno R, and Hori Y (2005) Spatial learning and long-term potentiation of mutant mice lacking 529-531. 3386-3391. amino acid oxidase activity and its implications for schizophrenia. Konno R and Yasumura Y (1992) 881-884. Tsai GE, Yang P, Chang YC, and Chong MY (2006) alanine in the brain of mutant mice lacking Depoortère R, Dargazanli G, Estenne-Bouhtou G, Coste A, Lanneau C, Desvignes C, Poncelet M, Heaulme M, Santucci V, Decobert M, et al. (2005) Neurochemical, electrophysiological and pharmacological profiles of the selective inhibitor of the glycine transporter-1 SSR504734, a potential new type of antipsychotic. 572-576. amino acid oxidase in schizophrenia. serine in several brain areas and periphery of rat. Institute of Laboratory Animal Resources (1996) serine nephrotoxic and alpha-aminoisobutyric acid protective? Hashimoto K, Engberg G, Shimizu E, Nordin C, Lindström LH, and Iyo M (2005) Reduced 480-482. Serine is an endogenous ligand for the glycine site of the Almond SL, Fradley RL, Armstrong EJ, Heavens RB, Rutter AR, Newman RJ, Chiu CS, Konno R, Hutson PH, and Brandon NJ (2006) Behavioral and biochemical characterization of a mutant mouse strain lacking 455-467. 41-48. serine to total serine ratio in the cerebrospinal fluid of drug naive schizophrenic patients. amino-acid oxidase. Johnson JW and Ascher P (1987) Glycine potentiates the NMDA response in cultured mouse brain neurons. Serine added to antipsychotics for the treatment of schizophrenia. 277-285. 7586-7591. 827-844. 214-220. Chumakov I, Blumenfeld M, Guerassimenko O, Cavarec L, Palicio M, Abderrahim H, Bougueleret L, Barry C, Tanaka H, La Rosa P, et al. (2002) Genetic and physiological data implicating the new human gene G72 and the gene for amino acids. Heresco-Levy U, Ermilov M, Shimoni J, Shapira B, Silipo G, and Javitt DC (2002) Placebo-controlled trial of Hashimoto A (2002) Effect of the intracerebroventricular and systemic administration of Moghaddam B (2003) Bringing order to the glutamate chaos in schizophrenia. serine D’Aniello A, D’Onofrio G, Pischetola M, D’Aniello G, Vetere A, Petrucelli L, and Fisher GH (1993) Biological role of cysteine and aspartate receptor hypofunction hypothesis of schizophrenia. 200-214. serine in patients with schizophrenia: evidence in support of the phthaldialdehyde. 9-12. Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Horowitz A, and Kelly D (1996) Double-blind, placebo-controlled, crossover trial of glycine adjuvant therapy for treatment-resistant schizophrenia. Hashimoto A, Nishikawa T, Oka T, Takahashi K, and Hayashi T (1992) Determination of free amino acid enantiomers in rat brain and serum by high-performance liquid chromatography after derivatization with tert.-butyloxycarbonyl- Rutter AR, Fradley RL, Garrett EM, Chapman KL, Lawrence JM, Rosahl TW, and Patel S (2007) Evidence from gene knockout studies implicates Asc-1 as the primary transporter mediating 119-125. 1757-1766. 481-487. Lane HY, Liu YC, Huang CL, Chang YC, Liau CH, Perng CH, and Tsai GE (2008) Sarcosine aspartate, and 610-617. 556-565. 1081-1089. 324-334. 4926-4931. Sparey T, Abeywickrema P, Almond S, Brandon N, Byrne N, Campbell A, Hutson PH, Jacobson M, Jones B, Munshi S, et al. (2008) The discovery of fused pyrrole carboxylic acids as novel, potent 33-36. and amino acid oxidase inhibitor with potential anti-psychotic properties. cycloserine added to conventional neuroleptics, olanzapine, or risperidone in schizophrenia. methylglycine) treatment for acute schizophrenia: a randomized, double-blind study. aspartate receptor. Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner JD, Heninger GR, Bowers MB Jr, and Charney DS (1994) Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: psychotomimetic, perceptual, cognitive, and neuroendocrine responses. alanine in the central nervous system and serum in mutant mice lacking Kemp JA and Leeson PD (1993) The glycine site of the NMDA receptor-five years on. 448-459. F382-F390. Smith KE, Borden LA, Hartig PR, Branchek T, and Weinshank RL (1992) Cloning and expression of a glycine transporter reveal colocalization with NMDA receptors. Tsai G, Yang P, Chung LC, Lange N, and Coyle JT (1998) Verrall L, Walker M, Rawlings N, Benzel I, Kew JN, Harrison PJ, and Burnet PW (2007) 1657-1669. Hashimoto K, Fukushima T, Shimizu E, Komatsu N, Watanabe H, Shinoda N, Nakazato M, Kumakiri C, Okada S, Hasegawa H, et al. (2003) Decreased serum levels of Morikawa A, Hamase K, Inoue T, Konno R, Niwa A, and Zaitsu K (2001) Determination of free Cubelos B, Giménez C, and Zafra F (2005) Localization of the GLYT1 glycine transporter at glutamatergic synapses in the rat brain. 927-935. Heresco-Levy U (2005) Glutamatergic neurotransmission modulators as emerging new drugs for schizophrenia. Mothet JP, Parent AT, Wolosker H, Brady RO Jr, Linden DJ, Ferris CD, Rogawski MA, and Snyder SH (2000) 767-769. Kapur S and Mamo D (2003) Half a century of antipsychotics and still a central role for dopamine D2 receptors. [3-(4′-fluorophenyl)-3-(4′-phenylphenoxy)propyl]sarcosine potentiates NMDA receptor-mediated responses in vivo and produces an antipsychotic profile in rodent behavior. Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Silipo G, and Lichtenstein M (1999) Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia. Brandish PE, Chiu CS, Schneeweis J, Brandon NJ, Leech CL, Kornienko O, Scolnick EM, Strulovici B, and Zheng W (2006) A cell-based ultra-high-throughput screening assay for identifying inhibitors of amino acid oxidase activity. 1963-1985. serine on the concentrations of 10.1124/jpet.108.147884_bib18 10.1124/jpet.108.147884_bib17 10.1124/jpet.108.147884_bib39 10.1124/jpet.108.147884_bib16 10.1124/jpet.108.147884_bib38 10.1124/jpet.108.147884_bib15 10.1124/jpet.108.147884_bib37 10.1124/jpet.108.147884_bib19 10.1124/jpet.108.147884_bib5 10.1124/jpet.108.147884_bib10 10.1124/jpet.108.147884_bib32 10.1124/jpet.108.147884_bib4 10.1124/jpet.108.147884_bib31 10.1124/jpet.108.147884_bib7 10.1124/jpet.108.147884_bib30 10.1124/jpet.108.147884_bib6 10.1124/jpet.108.147884_bib9 10.1124/jpet.108.147884_bib14 10.1124/jpet.108.147884_bib36 10.1124/jpet.108.147884_bib8 10.1124/jpet.108.147884_bib13 10.1124/jpet.108.147884_bib35 10.1124/jpet.108.147884_bib12 10.1124/jpet.108.147884_bib34 10.1124/jpet.108.147884_bib11 10.1124/jpet.108.147884_bib33 10.1124/jpet.108.147884_bib1 10.1124/jpet.108.147884_bib3 10.1124/jpet.108.147884_bib2 10.1124/jpet.108.147884_bib29 10.1124/jpet.108.147884_bib28 10.1124/jpet.108.147884_bib27 10.1124/jpet.108.147884_bib26 10.1124/jpet.108.147884_bib21 10.1124/jpet.108.147884_bib20 10.1124/jpet.108.147884_bib41 10.1124/jpet.108.147884_bib40 10.1124/jpet.108.147884_bib25 10.1124/jpet.108.147884_bib24 10.1124/jpet.108.147884_bib23 10.1124/jpet.108.147884_bib22 |
References_xml | – reference: 9-12. – reference: Mothet JP, Parent AT, Wolosker H, Brady RO Jr, Linden DJ, Ferris CD, Rogawski MA, and Snyder SH (2000) – reference: Tsai G, Lane HY, Yang P, Chong MY, and Lange N (2004) Glycine transporter I inhibitor, – reference: Verrall L, Walker M, Rawlings N, Benzel I, Kew JN, Harrison PJ, and Burnet PW (2007) – reference: Lane HY, Liu YC, Huang CL, Chang YC, Liau CH, Perng CH, and Tsai GE (2008) Sarcosine ( – reference: Morikawa A, Hamase K, Inoue T, Konno R, Niwa A, and Zaitsu K (2001) Determination of free – reference: 33-36. – reference: -methylglycine (sarcosine), added to antipsychotics for the treatment of schizophrenia. – reference: Hashimoto A, Nishikawa T, Oka T, Takahashi K, and Hayashi T (1992) Determination of free amino acid enantiomers in rat brain and serum by high-performance liquid chromatography after derivatization with – reference: Chumakov I, Blumenfeld M, Guerassimenko O, Cavarec L, Palicio M, Abderrahim H, Bougueleret L, Barry C, Tanaka H, La Rosa P, et al. (2002) Genetic and physiological data implicating the new human gene G72 and the gene for – reference: Hashimoto K, Engberg G, Shimizu E, Nordin C, Lindström LH, and Iyo M (2005) Reduced – reference: -Amino-acid oxidase and its physiological function. – reference: -cycloserine added to conventional neuroleptics, olanzapine, or risperidone in schizophrenia. – reference: McBain CJ, Kleckner NW, Wyrick S, and Dingledine R (1989) Structural requirements for activation of the glycine coagonist site of – reference: 230-234. – reference: Kinney GG, Sur C, Burno M, Mallorga PJ, Williams JB, Figueroa DJ, Wittmann M, Lemaire W, and Conn PJ (2003) The glycine transporter type 1 inhibitor – reference: 881-884. – reference: -amino acid oxidase activity and its implications for schizophrenia. – reference: -serine nephrotoxic and alpha-aminoisobutyric acid protective? – reference: -aminoacid oxidase as genetic risk factors for schizophrenia and bipolar affective disorder. – reference: 481-487. – reference: 455-467. – reference: -[3-(4′-fluorophenyl)-3-(4′-phenylphenoxy)propyl]sarcosine potentiates NMDA receptor-mediated responses in vivo and produces an antipsychotic profile in rodent behavior. – reference: Konno R and Yasumura Y (1992) – reference: Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Silipo G, and Lichtenstein M (1999) Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia. – reference: - and – reference: -serine to total serine ratio in the cerebrospinal fluid of drug naive schizophrenic patients. – reference: 1757-1766. – reference: 34-38. – reference: Tsai GE, Yang P, Chang YC, and Chong MY (2006) – reference: 13675-13680. – reference: 1081-1090. – reference: 452-456. – reference: 324-334. – reference: -phthaldialdehyde. – reference: -serine and – reference: 927-935. – reference: -serine in patients with schizophrenia: evidence in support of the – reference: Moghaddam B (2003) Bringing order to the glutamate chaos in schizophrenia. – reference: Heresco-Levy U, Ermilov M, Shimoni J, Shapira B, Silipo G, and Javitt DC (2002) Placebo-controlled trial of – reference: 199-214. – reference: -aspartate receptor hypofunction hypothesis of schizophrenia. – reference: 827-844. – reference: 41-48. – reference: 20-25. – reference: Kapur S and Mamo D (2003) Half a century of antipsychotics and still a central role for dopamine D2 receptors. – reference: Javitt DC (1987) Negative schizophrenic symptomatology and the PCP (phencyclidine) model of schizophrenia. – reference: -Serine added to antipsychotics for the treatment of schizophrenia. – reference: Institute of Laboratory Animal Resources (1996) – reference: -aspartate receptors expressed in Xenopus oocytes. – reference: 1963-1985. – reference: 12-35. – reference: 26941-26949. – reference: Depoortère R, Dargazanli G, Estenne-Bouhtou G, Coste A, Lanneau C, Desvignes C, Poncelet M, Heaulme M, Santucci V, Decobert M, et al. (2005) Neurochemical, electrophysiological and pharmacological profiles of the selective inhibitor of the glycine transporter-1 SSR504734, a potential new type of antipsychotic. – reference: -aspartate oxidase: effects of – reference: -tert.-butyloxycarbonyl- – reference: Heresco-Levy U, Javitt DC, Ermilov M, Mordel C, Horowitz A, and Kelly D (1996) Double-blind, placebo-controlled, crossover trial of glycine adjuvant therapy for treatment-resistant schizophrenia. – reference: Adage T, Trillat AC, Quattropani A, Perrin D, Cavarec L, Shaw J, Guerassimenko O, Giachetti C, Gréco B, Chumakov I, et al. (2008) In vitro and in vivo pharmacological profile of AS057278, a selective – reference: -aspartic acid, – reference: -cysteine and – reference: 203-207. – reference: Sparey T, Abeywickrema P, Almond S, Brandon N, Byrne N, Campbell A, Hutson PH, Jacobson M, Jones B, Munshi S, et al. (2008) The discovery of fused pyrrole carboxylic acids as novel, potent – reference: 3386-3391. – reference: Cubelos B, Giménez C, and Zafra F (2005) Localization of the GLYT1 glycine transporter at glutamatergic synapses in the rat brain. – reference: 200-214. – reference: 519-524. – reference: -serine reuptake in the mouse CNS. – reference: 7586-7591. – reference: -amino acid oxidase and – reference: Krystal JH, Karper LP, Seibyl JP, Freeman GK, Delaney R, Bremner JD, Heninger GR, Bowers MB Jr, and Charney DS (1994) Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans: psychotomimetic, perceptual, cognitive, and neuroendocrine responses. – reference: 480-482. – reference: -alanine in the brain of mutant mice lacking – reference: Smith KE, Borden LA, Hartig PR, Branchek T, and Weinshank RL (1992) Cloning and expression of a glycine transporter reveal colocalization with NMDA receptors. – reference: -amino acid oxidase inhibitor with potential anti-psychotic properties. – reference: 448-459. – reference: Hashimoto K, Fukushima T, Shimizu E, Komatsu N, Watanabe H, Shinoda N, Nakazato M, Kumakiri C, Okada S, Hasegawa H, et al. (2003) Decreased serum levels of – reference: -amino acid oxidase in schizophrenia. – reference: -serine on the concentrations of – reference: -amino-acid oxidase. – reference: -aspartate receptor. – reference: -amino acid oxidase (DAO) inhibitors. – reference: Hashimoto A, Nishikawa T, Konno R, Niwa A, Oka T, and Takahashi K (1993) Free – reference: Konno R and Yasumura Y (1983) Mouse mutant deficient in – reference: Almond SL, Fradley RL, Armstrong EJ, Heavens RB, Rutter AR, Newman RJ, Chiu CS, Konno R, Hutson PH, and Brandon NJ (2006) Behavioral and biochemical characterization of a mutant mouse strain lacking – reference: F382-F390. – reference: -methylglycine) treatment for acute schizophrenia: a randomized, double-blind study. – reference: 4926-4931. – reference: 214-220. – reference: , 7th ed. Institute of Laboratory Animal Resources, Commission on Life Sciences, National Research Council, Washington, DC. – reference: 1657-1669. – reference: D’Aniello A, D’Onofrio G, Pischetola M, D’Aniello G, Vetere A, Petrucelli L, and Fisher GH (1993) Biological role of – reference: -Alanine added to antipsychotics for the treatment of schizophrenia. – reference: Tsai G, Yang P, Chung LC, Lange N, and Coyle JT (1998) – reference: 277-285. – reference: 119-125. – reference: Brandish PE, Chiu CS, Schneeweis J, Brandon NJ, Leech CL, Kornienko O, Scolnick EM, Strulovici B, and Zheng W (2006) A cell-based ultra-high-throughput screening assay for identifying inhibitors of – reference: Krug AW, Völker K, Dantzler WH, and Silbernagl S (2007) Why is – reference: -serine in several brain areas and periphery of rat. – reference: Rutter AR, Fradley RL, Garrett EM, Chapman KL, Lawrence JM, Rosahl TW, and Patel S (2007) Evidence from gene knockout studies implicates Asc-1 as the primary transporter mediating – reference: -methyl- – reference: Schumacher J, Jamra RA, Freudenberg J, Becker T, Ohlraun S, Otte AC, Tullius M, Kovalenko S, Bogaert AV, Maier W, et al. (2004) Examination of G72 and – reference: -alanine in the central nervous system and serum in mutant mice lacking – reference: 767-769. – reference: -Amino acid oxidase and serine racemase in human brain: normal distribution and altered expression in schizophrenia. – reference: 610-617. – reference: Maekawa M, Watanabe M, Yamaguchi S, Konno R, and Hori Y (2005) Spatial learning and long-term potentiation of mutant mice lacking – reference: 1081-1089. – reference: -serine, – reference: -Serine is an endogenous ligand for the glycine site of the – reference: Johnson JW and Ascher P (1987) Glycine potentiates the NMDA response in cultured mouse brain neurons. – reference: 29-36. – reference: Hashimoto A (2002) Effect of the intracerebroventricular and systemic administration of – reference: -amino acid oxidase. – reference: Lahti AC, Weiler MA, Tamara Michaelidis BA, Parwani A, and Tamminga CA (2001) Effects of ketamine in normal and schizophrenic volunteers. – reference: 572-576. – reference: Heresco-Levy U (2005) Glutamatergic neurotransmission modulators as emerging new drugs for schizophrenia. – reference: -aspartate, and – reference: -amino acids. – reference: -amino acid oxidase activity. – reference: 556-565. – reference: Kemp JA and Leeson PD (1993) The glycine site of the NMDA receptor-five years on. – reference: : 529-531. – ident: 10.1124/jpet.108.147884_bib2 doi: 10.1016/j.mcn.2006.05.003 – ident: 10.1124/jpet.108.147884_bib22 doi: 10.1523/JNEUROSCI.23-20-07586.2003 – ident: 10.1124/jpet.108.147884_bib3 doi: 10.1177/1087057106288181 – ident: 10.1124/jpet.108.147884_bib11 doi: 10.1016/j.pnpbp.2005.04.023 – ident: 10.1124/jpet.108.147884_bib13 doi: 10.1517/14728214.10.4.827 – ident: 10.1124/jpet.108.147884_bib40 doi: 10.1016/S0006-3223(98)00279-0 – ident: 10.1124/jpet.108.147884_bib7 doi: 10.1038/sj.npp.1300772 – ident: 10.1124/jpet.108.147884_bib36 doi: 10.1016/0896-6273(92)90207-T – ident: 10.1124/jpet.108.147884_bib18 – ident: 10.1124/jpet.108.147884_bib12 doi: 10.1001/archpsyc.60.6.572 – ident: 10.1124/jpet.108.147884_bib35 doi: 10.1038/sj.mp.4001421 – ident: 10.1124/jpet.108.147884_bib38 doi: 10.1016/j.biopsych.2003.09.012 – ident: 10.1124/jpet.108.147884_bib41 doi: 10.1111/j.1460-9568.2007.05769.x – ident: 10.1124/jpet.108.147884_bib21 doi: 10.1016/0165-6147(93)90108-V – ident: 10.1124/jpet.108.147884_bib23 doi: 10.1093/genetics/103.2.277 – ident: 10.1124/jpet.108.147884_bib20 doi: 10.1016/j.pnpbp.2003.09.004 – ident: 10.1124/jpet.108.147884_bib4 doi: 10.1073/pnas.182412499 – ident: 10.1124/jpet.108.147884_bib28 doi: 10.1016/j.biopsych.2007.04.038 – ident: 10.1124/jpet.108.147884_bib29 doi: 10.1016/j.neures.2005.05.008 – ident: 10.1124/jpet.108.147884_bib16 doi: 10.1001/archpsyc.56.1.29 – ident: 10.1124/jpet.108.147884_bib30 doi: 10.1016/S0026-895X(25)09633-6 – ident: 10.1124/jpet.108.147884_bib37 doi: 10.1016/j.bmcl.2008.04.020 – ident: 10.1124/jpet.108.147884_bib6 doi: 10.1016/S0021-9258(19)74201-X – ident: 10.1124/jpet.108.147884_bib15 doi: 10.1192/bjp.169.5.610 – ident: 10.1124/jpet.108.147884_bib8 doi: 10.1016/S0006-8993(02)03466-2 – ident: 10.1124/jpet.108.147884_bib32 doi: 10.1016/S0378-4347(01)00131-1 – ident: 10.1124/jpet.108.147884_bib9 doi: 10.1016/0304-3940(93)90476-2 – ident: 10.1124/jpet.108.147884_bib17 – ident: 10.1124/jpet.108.147884_bib27 doi: 10.1016/S0893-133X(01)00243-3 – ident: 10.1124/jpet.108.147884_bib33 doi: 10.1073/pnas.97.9.4926 – ident: 10.1124/jpet.108.147884_bib31 doi: 10.1016/S0896-6273(03)00757-8 – ident: 10.1124/jpet.108.147884_bib26 doi: 10.1001/archpsyc.1994.03950030035004 – ident: 10.1124/jpet.108.147884_bib34 doi: 10.1111/j.1460-9568.2007.05446.x – ident: 10.1124/jpet.108.147884_bib5 doi: 10.1093/cercor/bhh147 – ident: 10.1124/jpet.108.147884_bib24 doi: 10.1016/0020-711X(92)90322-R – ident: 10.1124/jpet.108.147884_bib14 doi: 10.1176/appi.ajp.159.3.480 – ident: 10.1124/jpet.108.147884_bib39 doi: 10.1016/j.biopsych.2005.06.032 – ident: 10.1124/jpet.108.147884_bib1 doi: 10.1016/j.euroneuro.2007.06.006 – ident: 10.1124/jpet.108.147884_bib10 doi: 10.1016/0378-4347(92)80300-F – ident: 10.1124/jpet.108.147884_bib19 doi: 10.1038/325529a0 – ident: 10.1124/jpet.108.147884_bib25 doi: 10.1152/ajprenal.00441.2006 |
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Snippet | Multiple studies indicate that N-methyl-d-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for... Multiple studies indicate that N -methyl- d -aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach... Multiple studies indicate that N-methyl-D-aspartate (NMDA) receptor hypofunction underlies some of the deficits associated with schizophrenia. One approach for... |
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SubjectTerms | Aged Animals D-Amino-Acid Oxidase - pharmacology Dizocilpine Maleate - pharmacology Habituation, Psychophysiologic Humans Male Models, Molecular Pyrroles - pharmacology Rats Rats, Wistar Recognition, Psychology - drug effects Schizophrenia - blood Schizophrenia - cerebrospinal fluid Serine - blood Serine - cerebrospinal fluid Serine - pharmacology Thiophenes - chemistry Thiophenes - pharmacology |
Title | The Behavioral and Neurochemical Effects of a Novel d-Amino Acid Oxidase Inhibitor Compound 8 [4 H-Thieno [3,2-b]pyrrole-5-carboxylic Acid] and d-Serine |
URI | https://dx.doi.org/10.1124/jpet.108.147884 http://jpet.aspetjournals.org/content/328/3/921.abstract https://www.ncbi.nlm.nih.gov/pubmed/19088300 |
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