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Dysregulation of the mesolimbic\u2010dopamine (<jats:styled-content style=\"fixed-case\">ML\u2010DA<\/jats:styled-content>) system is linked to these syndromes and<jats:styled-content style=\"fixed-case\">LTCCs<\/jats:styled-content>are required for normal<jats:styled-content style=\"fixed-case\">DAergic<\/jats:styled-content>neurotransmission between the ventral tegmental area (<jats:styled-content style=\"fixed-case\">VTA<\/jats:styled-content>) and nucleus accumbens (<jats:styled-content style=\"fixed-case\">NAc<\/jats:styled-content>). It is unclear, however, how variations in<jats:italic><jats:styled-content style=\"fixed-case\">CACNA1C<\/jats:styled-content><\/jats:italic>genotype, and potential subsequent changes in expression levels in these regions, modify risk. Using constitutive and conditional knockout mice, and treatment with the<jats:styled-content style=\"fixed-case\">LTCC<\/jats:styled-content>antagonist nimodipine, we examined the role of<jats:italic>Cacna1c<\/jats:italic>in<jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>\u2010mediated behaviors elicited by psychomotor stimulants. Using fast\u2010scan cyclic voltammetry,<jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>release and reuptake in the<jats:styled-content style=\"fixed-case\">NAc<\/jats:styled-content>were measured. We find that subsecond<jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>release in<jats:italic>Cacna1c<\/jats:italic>haploinsufficient mice lacks normal sensitivity to inhibition of the<jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>transporter (<jats:styled-content style=\"fixed-case\">DAT<\/jats:styled-content>). Constitutive haploinsufficiency of<jats:italic>Cacna1c<\/jats:italic>led to attenuation of hyperlocomotion following acute administration of stimulants specific to<jats:styled-content style=\"fixed-case\">DAT<\/jats:styled-content>, and locomotor sensitization of these mice to the<jats:styled-content style=\"fixed-case\">DAT<\/jats:styled-content>antagonist<jats:styled-content style=\"fixed-case\">GBR12909<\/jats:styled-content>did not reach the same level as wild\u2010type mice. The maintenance of sensitization to<jats:styled-content style=\"fixed-case\">GBR12909<\/jats:styled-content>was attenuated by administration of nimodipine. Sensitization to<jats:styled-content style=\"fixed-case\">GBR12909<\/jats:styled-content>was attenuated in mice with reduced<jats:italic>Cacna1c<\/jats:italic>selectively in the<jats:styled-content style=\"fixed-case\">VTA<\/jats:styled-content>but not in the<jats:styled-content style=\"fixed-case\">NAc<\/jats:styled-content>. Our findings show that<jats:italic>Cacna1c<\/jats:italic>is crucial for normal behavioral responses to<jats:styled-content style=\"fixed-case\">DA<\/jats:styled-content>stimulants and that its activity in the<jats:styled-content style=\"fixed-case\">VTA<\/jats:styled-content>is required for behavioral sensitization.<jats:italic>Cacna1c<\/jats:italic>likely exerts these effects through modifications to presynaptic<jats:styled-content style=\"fixed-case\">ML\u2010DA<\/jats:styled-content>system function.<\/jats:p>","DOI":"10.1111\/gbb.12371","type":"journal-article","created":{"date-parts":[[2017,2,10]],"date-time":"2017-02-10T15:28:46Z","timestamp":1486740526000},"page":"495-505","source":"Crossref","is-referenced-by-count":35,"title":["Reduced levels of<i><scp>C<\/scp>acna1c<\/i>attenuate mesolimbic dopamine system function"],"prefix":"10.1111","volume":"16","author":[{"given":"C. E.","family":"Terrillion","sequence":"first","affiliation":[{"name":"Department of Psychiatry University of Maryland School of Medicine Baltimore MD USA"},{"name":"Program in Neuroscience University of Maryland School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D. T.","family":"Dao","sequence":"additional","affiliation":[{"name":"Department of Psychiatry University of Maryland School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"Cachope","sequence":"additional","affiliation":[{"name":"Department of Anatomy and Neurobiology University of Maryland School of Medicine Baltimore MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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