TY - JOUR T1 - Aetiology of bipolar disorder: contribution of the L-type voltage-gated calcium channels JF - General Psychiatry JO - Gen Psych DO - 10.1136/gpsych-2018-100009 VL - 32 IS - 2 SP - e100009 AU - Xiaoyun Guo AU - Dengtang Liu AU - Tong Wang AU - Xingguang Luo Y1 - 2019/07/01 UR - http://gpsych.bmj.com/content/32/2/e100009.abstract N2 - Bipolar disorder (BPD) is a common mental illness with significant morbidity and mortality.1 Although evidence have suggested changes in oxidative stress, dopamine and inflammation in BPD, it is hard to define the aetiological mechanism of BPD clearly. Recently, some but not all candidate gene association studies, family-based association studies, linkage studies, genome-wide association studies (GWASs) and meta-analyses showed that mutation of L-type voltage-gated calcium channels (LTCCs) gene CACNA1C is implicated in the mechanism of BPD.2–8 These findings support the possibility that BPD might have calcium channelopathy.9LTCCs, which consist of a complex of alpha-1, alpha-2/delta and beta subunits in a 1:1:1 ratio, mediate the influx of calcium ions (Ca2+) into the cell on membrane polarization. The alpha-1 subunit consists of 24 transmembrane segments and forms the pore through which ions pass into the cell. Cav1.2 is crucial in modulating kinetics of the LTCCs.10 Cav1.2 is widely expressed in the heart11 12 and brain.13 So far, it is well known for its function in the heart.11 12 LTCCs are located at both presynaptic nerve terminals and postsynaptic dendrites and dendritic spines. It initiates many physiological responses, including secretion, muscle contraction and gene transcription.LTCCs have prominent roles in learning and memory processes, which might be related with the pathology of BPD.14 LTCCs might control gene expression through … ER -