Past and Future Explanations for Depersonalization and Derealization Disorder: A Role for Predictive Coding.

Depersonalization (DP) and derealization (DR) refer to states of dissociation in which one feels a sense of alienation in relation to one's self and environment, respectively. Whilst transient episodes often diminish without treatment, chronic experiences of DP and DR may last for years, with common treatments lacking a strong evidence base for their efficacy. We propose a theoretical explanation of DP and DR based on interoceptive predictive coding, and discuss how transient experiences of DP and DR may be induced in the non-clinical population using virtual reality. Further, we review the use of heartbeat evoked potentials in detecting the neural correlates of DP and DR allowing for an objective measure of these experiences in the non-clinical population. Finally, we discuss how the induction and detection of transient experiences of DP and DR in the non-clinical population could shed light on how the brain constructs one's sense of self and reality.

NZO-3 expression causes global changes to actin cytoskeleton in Madin-Darby canine kidney cells: linking a tight junction protein to Rho GTPases.

We previously demonstrated that exogenous expression of a truncated form of the tight junction protein ZO-3 affected junctional complex assembly and function. Current results indicate that this ZO-3 construct influences actin cytoskeleton dynamics more globally. We show that expression of the amino-terminal half of ZO-3 (NZO-3) in Madin-Darby canine kidney cells results in a decreased number of stress fibers and focal adhesions and causes an increased rate of cell migration in a wound healing assay. We also demonstrate that RhoA activity is reduced in NZO-3-expressing cells. We determined that ZO-3 interacts with p120 catenin and AF-6, proteins localized to the junctional complex and implicated in signaling pathways important for cytoskeleton regulation and cell motility. We also provide evidence that NZO-3 interacts directly with the C terminus of ZO-3, and we propose a model where altered interactions between ZO-3 and p120 catenin in NZO-3-expressing cells affect RhoA GTPase activity. This study reveals a potential link between ZO-3 and RhoA-related signaling events.