Abstracts

We have recently described the first in vivo model of posttraumatic epilepsy (PTE) in the rat where chronic recurrent seizures appear following a single episode of rostral lateral fluid percussion injury (rpFPI; D[rsquo]Ambrosio et al., 2003). The frontal-parietal (FP) cortex is an early epileptic focus. To begin the identification of the epileptogenic mechanisms responsible for its onset we have examined the electrophysiological properties of FP glia before the epileptic condition arises. Severe rpFPI was induced in 29-32 days old male Sprague Dawley rats. Coronal slices were obtained 1 day post-injury. Whole cell patch clamp recordings were performed from FP cortex (bregma 0 though -4mm). Bath application of Ba²⁺ (40 [mu]M) was used to block K[sub]IR[/sub] channels. Cells were chosen from neocortical layers IV-VI. Data are shown as mean[plusmn]S.E.M. There was a significant loss in K[sub]IR[/sub] currents in FP glial cells 1 day post-rpFPI. Barium[ndash]sensitive current at -140mV represented 17.2[plusmn]2.9% of the whole cell current in na[iuml]ve glial cells (n=9), but only 8.0[plusmn]2.1% in injured glial cells (n=9; p[lt]=0.02 with Wilcoxon test). Our results demonstrated post-traumatic loss in glial K[sub]IR[/sub] conductance in the FP cortex 1 day post-injury. Because glial K[sub]IR[/sub] channels are known to be involved in proper extracellular K⁺-homeostasis, and because the FP cortex later develops into an epileptic focus, the observed electrophysiological changes in FP glia are pro-epileptogenic. These results also demonstrate the utility of the rpFPI-induced PTE model in allowing putative epileptogenic mechanisms to be examined before the development of the epileptic focus.
- D[rsquo]Ambrosio, Faibanks, Fender, Doyle, Born, Miller (2003) Posttraumatic epilepsy following fluid percussion injury in the rat. Brain. 2003 Nov 7 [Epub ahead of print]. (Supported by NIH/NINDS NS 40823 (RD).)