channel-interacting protein KCNAB2, which is itself associated with neuronal excitability17 and epilepsy19. We interpret these data to mean that NEAT1 may provide a scaffolding function in the nucleus that upon neuronal activation, releases modulatory proteins to fine-tune the excitatory response. Furthermore, our findings also show that downregulation of NEAT1 may result in changes to the expression of multiple gene transcripts involved in ion channel function following neuronal activation. These data point to NEAT1-associated paraspeckles either directly (e.g. through the binding of pre-mRNAs or guiding mRNA modifications on these transcripts) or indirectly (e.g. through sequestering transcript modifying proteins or upstream transcription factors) exerting a broad effect on downstream ion channel associated function.
