RT Journal Article
SR Electronic
T1 Rapid, Coordinate Inflammatory Responses after Experimental Febrile Status Epilepticus: Implications for Epileptogenesis
JF eneuro
JO eneuro
FD Society for Neuroscience
SP ENEURO.0034-15.2015
DO 10.1523/ENEURO.0034-15.2015
VO 2
IS 5
A1 Katelin P. Patterson
A1 Gary P. Brennan
A1 Megan Curran
A1 Eli Kinney-Lang
A1 Celine Dubé
A1 Faisal Rashid
A1 Catherine Ly
A1 Andre Obenaus
A1 Tallie Z. Baram
YR 2015
UL http://www.eneuro.org/content/2/5/ENEURO.0034-15.2015.abstract
AB Epilepsy is a common neurological disorder with many causes. For temporal lobe epilepsy, antecedent insults are typically found. These risk factors include trauma or history of long fever-associated seizures (febrile status epilepticus) in childhood. Whereas the mechanisms by which such insults promote temporal lobe epilepsy are unknown, an extensive body of work has implicated inflammation and inflammatory mediators in both human and animal models of the disorder. However, direct evidence for an epileptogenic role for inflammation is lacking. Here we capitalized on a model where only a subgroup of insult-experiencing rodents develops epilepsy. We reasoned that if inflammation was important for generating epilepsy, then early inflammation should be more prominent in individuals destined to become epileptic compared with those that will not become epileptic. In addition, the molecular and temporal profile of inflammatory mediators would provide insights into which inflammatory pathways might be involved in the disease process. We examined inflammatory profiles in hippocampus and amygdala of individual rats and correlated them with a concurrent noninvasive, amygdalar magnetic resonance imaging epilepsy-predictive marker. We found significant individual variability in the expression of several important inflammatory mediators, but not in others. Of interest, a higher expression of a subset of hippocampal and amygdalar inflammatory markers within the first few hours following an insult correlated with the epilepsy-predictive signal. These findings suggest that some components of the inflammatory gene network might contribute to the process by which insults promote the development of temporal lobe epilepsy.