{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:57:40Z","timestamp":1790913460015,"version":"4.1.0"},"reference-count":60,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2014,1,13]],"date-time":"2014-01-13T00:00:00Z","timestamp":1389571200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Health Future Foundation"},{"DOI":"10.13039\/100000097","name":"National Center for Research Resources","doi-asserted-by":"crossref","award":["G20RR024001"],"award-info":[{"award-number":["G20RR024001"]}],"id":[{"id":"10.13039\/100000097","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2014,2]]},"abstract":"\n Background and Purpose<\/jats:title>\n \n Despite ample evidence supporting the\n \n N<\/jats:styled-content>\n <\/jats:italic>\n \u2010methyl\u2010\n d<\/jats:sc>\n \u2010aspartate receptor (\n NMDAR<\/jats:styled-content>\n ) hypofunction hypothesis of schizophrenia, progress in the development of effective therapeutics based on this hypothesis has been limited. Facilitation of NMDA receptor function by co\u2010agonists (\n d<\/jats:sc>\n \u2010serine or glycine) only partially alleviates the symptoms in schizophrenia; other means to facilitate\n NMDA<\/jats:styled-content>\n receptors are required. NMDA receptor sub\u2010types differ in their subunit composition, with varied\n GluN2<\/jats:styled-content>\n subunits (\n GluN2A<\/jats:styled-content>\n \u2010\n GluN2D<\/jats:styled-content>\n ) imparting different physiological, biochemical and pharmacological properties.\n CIQ<\/jats:styled-content>\n is a positive allosteric modulator that is selective for\n GluN2C<\/jats:styled-content>\n \/\n GluN2D<\/jats:styled-content>\n \u2010containing NMDA receptor\n s<\/jats:styled-content>\n (\n M<\/jats:styled-content>\n ullasseril\n et\u2009al<\/jats:italic>\n .).\n <\/jats:p>\n <\/jats:sec>\n \n Experimental Approach<\/jats:title>\n \n The effect of systemic administration of\n CIQ<\/jats:styled-content>\n was tested on impairment in prepulse inhibition (\n PPI<\/jats:styled-content>\n ), hyperlocomotion and stereotypy induced by i.p. administration of\n MK<\/jats:styled-content>\n \u2010801 and methamphetamine. The effect of\n CIQ<\/jats:styled-content>\n was also tested on\n MK<\/jats:styled-content>\n \u2010801\u2010induced impairment in working memory in\n Y<\/jats:styled-content>\n \u2010maze spontaneous alternation test.\n <\/jats:p>\n <\/jats:sec>\n \n Key Results<\/jats:title>\n \n We found that systemic administration of\n CIQ<\/jats:styled-content>\n (20\u2009mg\u00b7kg\n \u22121<\/jats:sup>\n , i.p.) in mice reversed\n MK<\/jats:styled-content>\n \u2010801 (0.15\u2009mg\u00b7kg\n \u22121<\/jats:sup>\n , i.p.)\u2010induced, but not methamphetamine (3\u2009mg\u00b7kg\n \u22121<\/jats:sup>\n , i.p.)\u2010induced, deficit in\n PPI<\/jats:styled-content>\n .\n MK<\/jats:styled-content>\n \u2010801 increased the startle amplitude to pulse alone, which was not reversed by\n CIQ<\/jats:styled-content>\n . In contrast, methamphetamine reduced the startle amplitude to pulse alone, which was reversed by\n CIQ<\/jats:styled-content>\n .\n CIQ<\/jats:styled-content>\n also partially attenuated\n MK<\/jats:styled-content>\n \u2010801\u2010 and methamphetamine\u2010induced hyperlocomotion and stereotyped behaviours. Additionally,\n CIQ<\/jats:styled-content>\n reversed the\n MK<\/jats:styled-content>\n \u2010801\u2010induced working memory deficit in spontaneous alternation in a\n Y<\/jats:styled-content>\n \u2010maze.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion and Implications<\/jats:title>\n \n Together, these results suggest that facilitation of\n GluN2C<\/jats:styled-content>\n \/\n GluN2D<\/jats:styled-content>\n \u2010containing receptors may serve as an important therapeutic strategy for treating positive and cognitive symptoms in schizophrenia.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/bph.12518","type":"journal-article","created":{"date-parts":[[2013,11,14]],"date-time":"2013-11-14T23:56:57Z","timestamp":1384473417000},"page":"799-809","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":95,"title":["GluN2C<\/scp>\n \/\n GluN2D<\/scp>\n subunit\u2010selective\n NMDA<\/scp>\n receptor potentiator\n CIQ<\/scp>\n reverses\n MK<\/scp>\n \u2010801\u2010induced impairment in prepulse inhibition and working memory in\n Y<\/scp>\n \u2010maze test in mice"],"prefix":"10.1111","volume":"171","author":[{"given":"P S","family":"Suryavanshi","sequence":"first","affiliation":[{"name":"Department of Pharmacology Creighton University Omaha NE USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R R","family":"Ugale","sequence":"additional","affiliation":[{"name":"Department of Pharmacology School of Pharmacy Guru Ghasidas Central University Bilaspur India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D","family":"Yilmazer\u2010Hanke","sequence":"additional","affiliation":[{"name":"Department of Biomedical Sciences Creighton University Omaha NE USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D J","family":"Stairs","sequence":"additional","affiliation":[{"name":"Department of Psychology Creighton University Omaha NE USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S M","family":"Dravid","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Creighton University Omaha NE 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