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Erythropoietin reduces epileptogenic processes following status epilepticus
Author(s) -
Chu Kon,
Jung KeunHwa,
Lee SoonTae,
Kim JinHee,
Kang KyungMuk,
Kim HyunKyung,
Lim JaeSung,
Park HeeKwon,
Kim Manho,
Lee Sang Kun,
Roh JaeKyu
Publication year - 2008
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2008.01644.x
Subject(s) - status epilepticus , erythropoietin , epilepsy , epileptogenesis , medicine , microglia , neuroscience , neurogenesis , glutamate receptor , pharmacology , inflammation , receptor , biology
Summary Purpose: Erythropoietin (EPO) has neuron and astroglial protective effects via reduction of tissue‐injuring molecules such as reactive oxygen species, glutamate, inflammatory cytokines, and other damaging molecules. Although EPO may constitute an effective therapeutic modality in cases of epileptic insult, no study has been performed on the effects of exogenous EPO on the chronic seizure formation. In this study, we attempted to investigate if EPO could modulate the altered microenvironment in the epileptic rat brain. Methods: Morphological changes in the hippocampi of rats subjected to lithium‐pilocarpine‐induced status epilepticus (SE) were examined with respect to neuronal loss, inflammation, blood–brain barrier (BBB) leakage, and cell genesis. Spontaneous recurrent seizures (SRSs) were investigated by long‐term video‐EEG monitoring. Results: EPO receptor (EPOR) was found to be increased in the hippocampus after SE. Administered EPO prevented, during the latent period following SE, BBB leakage, neuronal death, and microglia activation in the dentate hilus, CA1, and CA3, and inhibited the generation of ectopic granule cells in the hilus and new glia in CA1. Moreover, EPO reduced the risk of SRS development. Discussion: These findings suggest that EPO has a potential therapeutic role in the setting of acute epileptic insults.