NEAT1 is widely expressed in the human body and other studies have also reported an up-regulation of NEAT1 in response to other forms of chronic stress, for example, in the placenta of patients with Intrauterine Growth Restriction (IUGR)31, and in response to stressors such as proteasome degradation14 and viral infection1332. Therefore, it may be that NEAT1 regulates a common mechanism of activity-dependence and chronic stress-induced insensitivity whose functional specifics are contingent on cell-type. Such a function is consistent with the emerging view that lncRNAs act as molecular scaffolds through their binding to many cellular components7. Our results thus propose a novel and therapeutically relevant lncRNA-mediated molecular mechanism in human neurons. Future studies would be required to explore the ways in which NEAT1 may function as a common regulatory hub regulating signaling pathways linked to seizure states and other normal and pathological physiological conditions.
