Expression data from rat brain following ischemic stroke or undercut. Rattus norvegicus

Although it is well known that stroke and head trauma are one of the high risk factors for the development of acquired epilepsy, the cellular mechanisms underlying the epileptogenesis is not well understood. Using rodent models of ischemic stroke and head trauma (partial cortical isolation, undercut), we comparatively analyzed transcription profiles between two different models to explore the commonality. Despite well-known risk factors such as stroke and head trauma, it has not been clinically effective to prevent acquired epilepsy. To do so, it is crucial to understand what commonly drives neural hyperexcitability. Using comparative transcriptome analyses with different models of acquired epilepsy including stroke and head trauma (the present GEO case), as well as blood-brain barrier (BBB) disruption, albumin, and TGFβ application (GEO accession number: GSE12304), we show that TGFβ signaling activation following BBB disruption commonly occurs regardless of brain region and insult types, accompanied by the strong upregulation of genes relevant to inflammation and extracellular matrix (ECM) modulation. Overall design: For undercut: RNAs were extracted from rat cortices 24 hour after either partial cortical isolation (Undercut, UC; n=3) or sham operations (UC_Sham; n=3). For stroke: The infarction was induced by photothrombisis using Rose Bengal in the somatosensory cortex of rats. RNAs were extracted from ipsilateral hippocampi at three time points (n=1; 12h, 24h, and 7d). RNAs extracted from sham-operated animals served as control at each time point (n=1; 12h, 24h, and 7d).