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Experimental models of chemoconvulsant\u2010induced status epilepticus remain the models of choice to discover potential antiepileptogenic drugs, but doubts remain as to the extent to which they model human pathophysiology. The aim of the present study was to compare the molecular landscape of the intra\u2010amygdala kainic acid model of status epilepticus in mice with findings in resected brain tissue from patients with drug\u2010resistant temporal lobe epilepsy (TLE).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Status epilepticus was induced via intra\u2010amygdala microinjection of kainic acid in C57BL\/6 mice, and gene expression was analyzed via microarrays in hippocampal tissue at acute and chronic time\u2010points. Results were compared to reference datasets in the intraperitoneal pilocarpine and intrahippocampal kainic acid model and to human resected brain tissue (hippocampus and cortex) from patients with drug\u2010resistant TLE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Intra\u2010amygdala kainic acid injection in mice triggered extensive dysregulation of gene expression that was ~3\u2010fold greater shortly after status epilepticus (2729 genes) when compared to epilepsy (412). Comparison to samples from patients with TLE revealed a particularly high correlation of gene dysregulation during established epilepsy. Pathway analysis found suppression of calcium signaling to be highly conserved across different models of epilepsy and patients. cAMP response element\u2010binding protein (CREB) was predicted as one of the main upstream transcription factors regulating gene expression during acute and chronic phases, and inhibition of CREB reduced seizure severity in the intra\u2010amygdala kainic acid model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>Our findings suggest the intra\u2010amygdala kainic acid model faithfully replicates key molecular features of human drug\u2010resistant TLE and provides potential rational target approaches for disease\u2010modification through new insights into the unique and shared gene expression landscape in experimental epilepsy.<\/jats:p>\n                  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