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Biochemical, structural, and functional abnormalities in primary bipolar disorder could also occur secondary to seizure disorders. The kindling paradigm, invoked as a model for understanding seizure disorders, has also been applied to the episodic nature of bipolar disorder. In bipolar patients, changes in second-messenger systems, such as G-proteins, phosphatidylinositol, protein kinase C, myristoylated alanine-rich C kinase substrate, or calcium activity have been described, along with changes in c-fos expression. Common mechanisms at the level of ion channels might include the antikindling and the calcium-antagonistic and potassium outward current-modulating properties of antiepileptic drugs. All these lines of research appear to be converging on a richer understanding of neurobiological underpinnings between bipolar disorder and epilepsy. Mania, which is the other side of the coin in affective disorders, may represent a privileged window into the neurobiology of mood regulation and the neurobiology of epilepsy itself. Future research on intracellular mechanisms might become decisive for a better understanding of the similarities between these two disorders. NEUROSCIENTIST 13(4):392\u2014404, 2007. DOI: 10.1177\/1073858407301117<\/jats:p>","DOI":"10.1177\/10738584070130041101","type":"journal-article","created":{"date-parts":[[2007,7,20]],"date-time":"2007-07-20T16:13:02Z","timestamp":1184947982000},"page":"392-404","source":"Crossref","is-referenced-by-count":49,"title":["Bipolar Disorder and Epilepsy: A Bidirectional Relation? 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