Postmortem neuropathological studies uncovered many changes in the brains of subjects with BD and findings from BD animal models seemed to be consistent (Martinowich, Schloesser, & Manji, 2009). These changes include, hyperactivity in protein kinase A and C (PKA and PKC) pathways (Bezchlibnyk & Young, 2002; Chang, Li, & Warsh, 2003; H. Wang & Friedman, 2001), reduced glial cell number (Andreazza & Young, 2014) and perturbations in neurotransmission (Berk et al., 2007; Du, Quiroz, Yuan, Zarate, & Manji, 2004; Mahmood & Silverstone, 2001; Scarr, Pavey, Sundram, MacKinnon, & Dean, 2003). However, what causes these changes in a BD patient remains undetermined, making it difficult to understand the pathophysiology of BD. One widely prescribed therapy for BD is lithium, however, only a subpopulation of the BD patients responds to lithium while others are unresponsive. To accurately and comprehensively model BD, a recent study using an iPS cell model for human BD reported the cellular phenotypes of hippocampal dentate-gyrus like human neuronal cells from manic type I BD patient fibroblasts (Mertens, Wang, et al., 2015). Electrophysiology and Ca2+ imaging revealed hyperactive action
