{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T02:35:50Z","timestamp":1790994950393,"version":"4.1.0"},"reference-count":65,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,2,25]],"date-time":"2013-02-25T00:00:00Z","timestamp":1361750400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2013,3]]},"abstract":"Background and Purpose<\/jats:title>To evaluate the ability of cannabidiolic acid (CBDA<\/jats:styled-content>) to reduce nausea and vomiting and enhance 5\u2010HT1A<\/jats:sub><\/jats:styled-content> receptor activation in animal models.<\/jats:p><\/jats:sec>Experimental Approach<\/jats:title>We investigated the effect of CBDA<\/jats:styled-content> on (i) lithium chloride (LiCl<\/jats:styled-content>)\u2010induced conditioned gaping to a flavour (nausea\u2010induced behaviour) or a context (model of anticipatory nausea) in rats; (ii) saccharin palatability in rats; (iii) motion\u2010, LiCl<\/jats:styled-content>\u2010 or cisplatin\u2010induced vomiting in house musk shrews (S<\/jats:styled-content>uncus murinus<\/jats:italic>); and (iv) rat brainstem 5\u2010HT1A<\/jats:sub><\/jats:styled-content> receptor activation by 8\u2010hydroxy\u20102\u2010(di\u2010n<\/jats:italic>\u2010propylamino)tetralin (8\u2010OH\u2010DPAT<\/jats:styled-content>) and mouse whole brain CB<\/jats:styled-content>1<\/jats:sub> receptor activation by CP<\/jats:styled-content>55940, using [35<\/jats:sup>S<\/jats:styled-content>]GTP<\/jats:styled-content>\u03b3S<\/jats:styled-content>\u2010binding assays.<\/jats:p><\/jats:sec>Key Results<\/jats:title>In shrews, CBDA<\/jats:styled-content> (0.1 and\/or 0.5\u2009mg\u00b7kg\u22121<\/jats:sup> i.p.) reduced toxin\u2010 and motion\u2010induced vomiting, and increased the onset latency of the first motion\u2010induced emetic episode. In rats, CBDA<\/jats:styled-content> (0.01 and 0.1\u2009mg\u00b7kg\u22121<\/jats:sup> i.p.) suppressed LiCl<\/jats:styled-content>\u2010 and context\u2010induced conditioned gaping, effects that were blocked by the 5\u2010HT1A<\/jats:sub><\/jats:styled-content> receptor antagonist, WAY<\/jats:styled-content>100635 (0.1\u2009mg\u00b7kg\u22121<\/jats:sup> i.p.), and, at 0.01\u2009mg\u00b7kg\u22121<\/jats:sup> i.p., enhanced saccharin palatability. CBDA<\/jats:styled-content>\u2010induced suppression of LiCl<\/jats:styled-content>\u2010induced conditioned gaping was unaffected by the CB<\/jats:styled-content>1<\/jats:sub> receptor antagonist, SR141716A<\/jats:styled-content> (1\u2009mg\u00b7kg\u22121<\/jats:sup> i.p.). In vitro<\/jats:italic>, CBDA<\/jats:styled-content> (0.1\u2013100\u2009nM<\/jats:styled-content>) increased the E<\/jats:styled-content><\/jats:italic>max<\/jats:sub> of 8\u2010OH\u2010DPAT<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions and Implications<\/jats:title>Compared with cannabidiol, CBDA<\/jats:styled-content> displays significantly greater potency at inhibiting vomiting in shrews and nausea in rats, and at enhancing 5\u2010HT1A<\/jats:sub><\/jats:styled-content> receptor activation, an action that accounts for its ability to attenuate conditioned gaping in rats. Consequently, CBDA<\/jats:styled-content> shows promise as a treatment for nausea and vomiting, including anticipatory nausea for which no specific therapy is currently available.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.12043","type":"journal-article","created":{"date-parts":[[2012,11,2]],"date-time":"2012-11-02T11:37:34Z","timestamp":1351856254000},"page":"1456-1470","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":149,"title":["Cannabidiolic acid prevents vomiting in S<\/scp>uncus murinus<\/i> and nausea\u2010induced behaviour in rats by enhancing 5\u2010HT1A<\/sub><\/scp> receptor activation"],"prefix":"10.1111","volume":"168","author":[{"given":"D","family":"Bolognini","sequence":"first","affiliation":[{"name":"Institute of Medical Sciences University of Aberdeen Aberdeen UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"EM","family":"Rock","sequence":"additional","affiliation":[{"name":"Department of Psychology and Neuroscience Graduate Program University of Guelph Guelph ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"NL","family":"Cluny","sequence":"additional","affiliation":[{"name":"Department of Physiology and Pharmacology University of Calgary Calgary AB Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MG","family":"Cascio","sequence":"additional","affiliation":[{"name":"Institute of Medical Sciences University of Aberdeen Aberdeen UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"CL","family":"Limebeer","sequence":"additional","affiliation":[{"name":"Department of Psychology and Neuroscience Graduate Program University of Guelph Guelph ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Duncan","sequence":"additional","affiliation":[{"name":"Sovereign House GW Research Ltd Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"CG","family":"Stott","sequence":"additional","affiliation":[{"name":"Sovereign House GW Research Ltd Cambridge UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"FA","family":"Javid","sequence":"additional","affiliation":[{"name":"Division of Pharmacy and Pharmaceutical Sciences School of Applied Sciences University of Huddersfield Huddersfield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"LA","family":"Parker","sequence":"additional","affiliation":[{"name":"Department of Psychology and Neuroscience Graduate Program University of Guelph Guelph ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"RG","family":"Pertwee","sequence":"additional","affiliation":[{"name":"Institute of Medical Sciences University of Aberdeen Aberdeen UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2013,2,25]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M111.296020"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1186\/1477-7525-1-46"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/bjc.1997.507"},{"key":"e_1_2_8_5_1","unstructured":"BologniniD RockEM CascioMG ParkerL PertweeRG(2012).Cannabidiolic acid behaves as a highly potent enhancer of 5\u2010HT1Areceptor activation bothin vitroandin vivo.22nd Annual Symposium of the Cannabinoids. 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