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Summary   Objective  Studies have addressed the potential involvement of L‐12/15‐lipoxygenases ( LO s), a polyunsaturated fatty acid metabolizing enzyme, in experimental models of acute stroke and chronic neurodegeneration; however, none to our knowledge has explored its role in epilepsy development. Thus, this study characterizes the cell‐specific expression of L‐12/15  ‐LO  in the brain and examines its contribution to epileptogenesis.    Methods  L‐12/15‐ LO  messenger RNA ( mRNA)  and protein expression and activity were characterized via polymerase chain reaction ( PCR) , immunocytochemistry and  enzyme‐linked immunosorbent assay (ELISA) , respectively. To assess its role in epileptogenesis, L‐12/15  ‐LO ‐deficient mice and their wild‐type littermates were treated with pentylenetetrazole ( PTZ , ip) every other day for up to 43 days (kindling paradigm). The innate seizure threshold was assessed by the acute  PTZ ‐induced seizure response of naive mice.    Results  L‐12/15  ‐LO mRNA  is expressed in hippocampal and cortical tissue from wild‐type C57 BL /6 mice. In addition, it is physically and functionally expressed by microglia, neurons, and brain microvessel endothelial cells, but not by astrocytes. Mice deficient in L‐12/15  ‐LO  were resistant to  PTZ ‐induced kindling and demonstrated an elevated innate seizure threshold. Despite this, a significant increase in seizure‐related mortality was observed during the kindling paradigm in L‐12/15  ‐LO  nulls relative to their wild‐type littermates.    Significance  The present study is the first to detail the role of L‐12/15‐ LO  in the epileptogenic process. The results suggest that constitutive L‐12/15‐ LO  expression contributes to a lower innate set point for  PTZ  acute seizure generation, translating to higher rates of kindling acquisition. Nevertheless, increased seizure‐related deaths in mice lacking activity of L‐12/15‐ LO  suggests that its products may influence endogenous mechanisms involved in termination of seizure activity.

Mice lacking L‐12/15‐lipoxygenase show increased mortality during kindling despite demonstrating resistance to epileptogenesis