{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,29]],"date-time":"2026-08-29T07:27:40Z","timestamp":1787988460814,"version":"build-2784847793"},"reference-count":66,"publisher":"American Medical Association (AMA)","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Psychiatry"],"published-print":{"date-parts":[[2024,9,1]]},"abstract":"\n Importance<\/jats:title>\n \n The risk of mental disorders is consistently associated with variants in\n CACNA1C<\/jats:italic>\n (L-type calcium channel Cav1.2) but it is not known why these channels are critical to cognition, and whether they affect the layer III pyramidal cells in the dorsolateral prefrontal cortex that are especially vulnerable in cognitive disorders.\n <\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To examine the molecular mechanisms expressed in layer III pyramidal cells in primate dorsolateral prefrontal cortices.<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n The design included transcriptomic analyses from human and macaque dorsolateral prefrontal cortex, and connectivity, protein expression, physiology, and cognitive behavior in macaques. The research was performed in academic laboratories at Yale, Harvard, Princeton, and the University of Pittsburgh. As dorsolateral prefrontal cortex only exists in primates, the work evaluated humans and macaques.<\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n Outcome measures included transcriptomic signatures of human and macaque pyramidal cells, protein expression and interactions in layer III macaque pyramidal cells using light and electron microscopy, changes in neuronal firing during spatial working memory, and working memory performance following pharmacological treatments.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Layer III pyramidal cells in dorsolateral prefrontal cortex coexpress a constellation of calcium-related proteins, delineated by\n CALB1<\/jats:italic>\n (calbindin), and high levels of\n CACNA1C<\/jats:italic>\n (Cav1.2),\n GRIN2B<\/jats:italic>\n (NMDA receptor GluN2B), and\n KCNN3<\/jats:italic>\n (SK3 potassium channel), concentrated in dendritic spines near the calcium-storing smooth endoplasmic reticulum. L-type calcium channels influenced neuronal firing needed for working memory, where either blockade or increased drive by \u03b21-adrenoceptors, reduced neuronal firing by a mean (SD) 37.3% (5.5%) or 40% (6.3%), respectively, the latter via SK potassium channel opening. An L-type calcium channel blocker or \u03b21-adrenoceptor antagonist protected working memory from stress.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n \n The layer III pyramidal cells in the dorsolateral prefrontal cortex especially vulnerable in cognitive disorders differentially express calbindin and a constellation of calcium-related proteins including L-type calcium channels Cav1.2 (\n CACNA1C<\/jats:italic>\n ), GluN2B-NMDA receptors (\n GRIN2B<\/jats:italic>\n ), and SK3 potassium channels (\n KCNN3<\/jats:italic>\n ), which influence memory-related neuronal firing. The finding that either inadequate or excessive L-type calcium channel activation reduced neuronal firing explains why either loss- or gain-of-function variants in\n CACNA1C<\/jats:italic>\n were associated with increased risk of cognitive disorders. The selective expression of calbindin in these pyramidal cells highlights the importance of regulatory mechanisms in neurons with high calcium signaling, consistent with Alzheimer tau pathology emerging when calbindin is lost with age and\/or inflammation.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamapsychiatry.2024.1112","type":"journal-article","created":{"date-parts":[[2024,5,22]],"date-time":"2024-05-22T11:34:45Z","timestamp":1716377685000},"page":"870","source":"Crossref","is-referenced-by-count":42,"title":["Key Roles of\n CACNA1C<\/i>\n \/Cav1.2 and CALB1\/Calbindin in Prefrontal Neurons Altered in Cognitive Disorders"],"prefix":"10.1001","volume":"81","author":[{"given":"Dibyadeep","family":"Datta","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Yale University School of Medicine, New Haven, Connecticut"},{"name":"Department of Psychiatry, Yale University School of Medicine, New Haven, 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