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Summary   Objective  Prolyl oligopeptidase ( PREP ) has been implicated in neuroinflammatory processes and neuroplasticity and has been suggested as a target for the treatment of neurodegenerative disease. The aim of this investigation was to explore the involvement of  PREP  in the neuropathologic mechanisms relevant to temporal lobe epilepsy ( TLE ) using a  PREP  inhibitor in a well‐established rat model.    Methods   PREP  activity and expression was studied in Sprague‐Dawley rats 2 and 12 weeks following kainic acid–induced status epilepticus ( KASE ). Continuous video‐electroencephalography monitoring was performed for 2 weeks in the 12‐week cohort to identify a relationship of  PREP  expression/activity with epileptic seizures. In addition, the animals included in the 2‐week time point were treated with a specific inhibitor of  PREP ,  KYP ‐2047, or saline continuously, starting immediately after  SE .  PREP  activity and its expression were analyzed in rat brain by using enzyme kinetics and western blot. In addition, markers for microglial activation, astrogliosis, cell loss, and cell proliferation were evaluated.    Results  Enzymatic activity of  PREP  was unchanged following induction of  SE  after 2 and 12 weeks in rats.  PREP  activity in epileptic rats did not relate to the number of seizures/day at the 12‐week time point. Moreover, continuous inhibition of  PREP  for 2 weeks after  KASE  did not alter the  SE ‐mediated neuroinflammatory response, cell loss, or cell proliferation in the hippocampal subgranule zone measured at the 2‐week time point.    Significance   PREP  inhibition does not affect key pathologic mechanisms, including activation of glial cells, cell loss, and neural progenitor cell proliferation, in this  KASE  model of TLE. The results do not support a direct role of  PREP  in seizure burden during the chronic epilepsy period in this model.

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Spatiotemporal expression and inhibition of prolyl oligopeptidase contradict its involvement in key pathologic mechanisms of kainic acid–induced temporal lobe epilepsy in rats