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Adult mice were divided into five groups of six animals\/group. Group 1 (control) was administered saline (10 mL\/kg i.p.). Group 2 received <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content> (2 mg\/kg i.p.). Groups 3 and 4 received bromocriptine (<jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>, 2.5 mg\/kg s.c.) and <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> (1 mg\/kg s.c.), respectively, while group 5 received their combination. Groups 3\u20135 later received <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content> 30 min after initial treatments. Animals were subjected to neurobehavioural tests and euthanized 18 h later. <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>s were characterized by significant increase (<jats:italic>P<\/jats:italic> &lt; 0.001) in cataleptic behaviour and lowered (<jats:italic>P<\/jats:italic> &lt; 0.05) spontaneous activity reaction time in mice. There were also significant (<jats:italic>P<\/jats:italic> &lt; 0.001) increases in malondialdehyde levels and decreased locomotion plus learning and memory parameters (<jats:italic>P<\/jats:italic> &lt; 0.05\u20130.001). <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> pretreatment alone did not alleviate <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010induced motor deficits in the mice. While pretreatment with <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content> alone attenuated <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010associated catalepsy, its combination with <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> further protected mice against <jats:styled-content style=\"fixed-case\">NA<\/jats:styled-content>s. Furthermore, <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content> pretreatment did not affect <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010induced increase in malondialdehyde level, but <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content>+<jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> significantly (<jats:italic>P<\/jats:italic> &lt; 0.05) decreased malondialdehyde in the <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010treated rats. Reduced glutathione levels and activities of superoxide dismutase and catalase remained elevated in all treatment groups. In conclusion, data from this study suggest possible chemopreventive benefit of <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> alone or in combination with <jats:styled-content style=\"fixed-case\">BMC<\/jats:styled-content> against <jats:styled-content style=\"fixed-case\">CPZ<\/jats:styled-content>\u2010associated neurobehavioural deficits. The ameliorative effect of <jats:styled-content style=\"fixed-case\">AML<\/jats:styled-content> may be related to its antioxidant and\/or calcium channel blocking property.<\/jats:p>","DOI":"10.1111\/fcp.12267","type":"journal-article","created":{"date-parts":[[2017,1,20]],"date-time":"2017-01-20T05:27:28Z","timestamp":1484890048000},"page":"329-339","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Amlodipine, an L\u2010type calcium channel blocker, protects against chlorpromazine\u2010induced neurobehavioural deficits in mice"],"prefix":"10.1111","volume":"31","author":[{"given":"Oluwafemi E.","family":"Kale","sequence":"first","affiliation":[{"name":"Department of Pharmacology Benjamin Carson (Snr.) 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