Short communicationCyclooxygenase-2 expression in the hippocampus of genetically epilepsy susceptible El mice was increased after seizure
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Cited by (49)
Differential regulation of gene expression pathways with dexamethasone and ACTH after early life seizures
2022, Neurobiology of DiseaseCitation Excerpt :In contrast, the gene Ptgs2 (Cox2) is downregulated by ACTH post-ELS. This gene has been actively studied in the context of seizure disorders and other neurological diseases for the past two decades (Okada et al., 2001; Chen et al., 2002; Almalki et al., 2014). In 2002, Chen and colleagues observed that selective COX2 inhibitors decreased membrane excitability and decreased back propagation of action potential-induced Ca2+ influx, a key feature of LTP.
Galangin Prevents Increased Susceptibility to Pentylenetetrazol-Stimulated Seizures by Prostaglandin E2
2019, NeuroscienceCitation Excerpt :However, despite the important role of PGE2 in controlling neuronal excitability, little is known about its functions during seizures. Therefore, it is appropriate to propose that COX-2 overexpression, as demonstrated in epileptic patients and experimental models (Okada et al., 2001; Desjardins et al., 2003), may raise PGE2 levels and contribute to the appearance and/or increase in the number of crises (Takemiya et al., 2003). In agreement, Oliveira et al. (2008b) demonstrated that the anti-inflammatory celecoxib (selective COX-2 inhibitor) increased latency to PTZ-induced seizures in rats, and this protective effect was reversed by administrating intracerebroventricular PGE2 [10 ng/2 μl (i.c.v.)].
Aspirin attenuates spontaneous recurrent seizures and inhibits hippocampal neuronal loss, mossy fiber sprouting and aberrant neurogenesis following pilocarpine-induced status epilepticus in rats
2012, Brain ResearchCitation Excerpt :COXs are rate-limiting enzymes in PGs synthesis and are major targets of nonsteroidal anti-inflammatory drugs (NSAIDs) (Takemiya et al., 2007). An up-regulation of hippocampal COX-2 expression was observed in epileptic rats and in patients with TLE (Desjardins et al., 2003; Okada et al., 2001). More recent data indicates that the expression of COX-1 in microglia was also enhanced in the hippocampus and areas around the third ventricle during the progression of seizures (Tanaka et al., 2009).