in response to chronic pilocarpine-induced seizure activity interestingly disappeared (Fig. 4c), perhaps due to homeostatic feedback. Second, we employed the hippocampal-specific kainic acid-induced seizure rat model that also closely resembles features of TLE28. Here, we again saw an acute (24 hours) down-regulation of NEAT1 and a chronic (10 weeks) insensitivity to seizure activity (Fig. 4d). These results, therefore, unify our findings (i.e. acute, activity-dependent down-regulation of NEAT1) with that of the literature (i.e. loss of NEAT1 down-regulation in response to chronic cellular stressors1113). This suggests that in neurons, NEAT1 expression is down-regulated in response to acute stimulation but develops insensitivity upon chronic stimulation leading to an increased risk of seizure activity.
