Abstracts

Inflammatory process in response to an infection can cause febrile seizures (FS) consisting of hyperthermia. FS may promote the development of temporal lobe epilepsy. It has been shown that an inflammatory response in mice contributes to the onset of FS. On other hand, it has been shown in rats that FS is followed by long-term modification of brain excitability. To further examine whether FS results in modification of brain excitability, we induced an inflammatory response in combination with FS Hyperthermia was induced in rat pups at either P11 or P16 using a heating lamp which increased body temperature at a rate of 1[deg]C/min. Core temperature was continuously monitored using a rectal probe. Rat pups were maintain at the temperature seizure threshold during 5 min. In order to induce an inflammatory response, lipopolysaccharide (LPS, E. coli 055:B5) was injected i.p. at 5ug/kg or 50ug/kg, two hours prior the induction of the seizures. Six groups were studied: FS at P11 (P11FS), FS+LPS 5[mu]g/kg at P11 (P11LPS5), FS+LPS 50[mu]g/kg at P11 (P11LPS50), FS at P16 (P16FS), FS+LPS 5[mu]g/kg at P16 (P16LPS5), and FS+LPS 50[mu]g/kg at P16 (P16LPS50). After 1 month, pentylenetetrazol threshold (PTZth) was used to assess the modification of brain excitability (n = 8/group). PTZ was dissolved to obtain a concentration of 10mg/kg and was infused into the tail-vain at the rate of 5ml/h. Seizure threshold dose (mg/kg) was derived from the time of infusion required to achieve the first bilateral forelimb myoclonus The temperature thresholds to induce the first seizure were not different among the groups. The temperature thresholds were: 41.2[plusmn]0.3[deg]C in P11FS, 41.3[plusmn]0.3[deg]C in P16FS, 42.1[plusmn]0.2[deg]C in P11LPS5, 41.8[plusmn]0.3[deg]C in P16LPS5, 41.8[plusmn]0.7[deg]C in P11LPS50 and 42.2[plusmn]0.3[deg]C in P16LPS50.The mortality rate were : 9% in P11FS, 12% in P16FS, 17% in P11LPS5, 18% in P16LPS5, 20% in P11LPS50 and 40% in P16LPS50. The PTZth (mg/kg mean[plusmn]sem) were not significantly different among the sham and FS only groups, or across ages with LPS treatment at either age. With in each age group, however, the PTZth was significantly lowered after either dose of LPS (38.8[plusmn]1.2 in P11FS, 34.8[plusmn]0.8 in P11LPS5 and 32.9[plusmn]1.1 P11LPS50 [ p [lt] 0.05 ]and 38.1[plusmn]0.7 in P16FS, 34.5[plusmn]0.7 in P16LPS5, 33.6[plusmn]0.9 in P16LPS50 [p [lt]0.05]) Lower PTZth obtained by using LPS in combination with FS in rat pups suggests modification of brain excitability. P11 appears to be the most useful age to study FS after inflammation due to the higher mortality at the older age group. Previous studies have shown that 30 min of FS is required for enhanced excitability. Our model with only 5 min of FS in combination with LPS suggests that an inflammatory response could, in part, explain brain excitability following FS (Supported by AEAC association.)