Abstracts

Rationale: Interaction between sleep deprivation (SD) and epilepsy has been discussed in many studies. Nevertheless the underlying mechanisms concerning the real effect of SD on epilepsy remain controversial (Neurology 2002; 59(9): 1371). One of the most valuable experimental models in epilepsy is the induction of temporal lobe epilepsy by pilocarpine (Behav. Brain Res. 1983; 9(3):315. Our objective in this study was to evaluate the effects of paradoxical sleep deprivation (PSD) on the evolution of pilocarpine (PILO)-induced temporal lobe epilepsy. Methods: In the first phase of the experiment, adult male Wistar rats (N=140) were divided in two groups: GI) Paradoxical sleep deprivation (PSD) group (N=70): animals submitted to PSD in a single platform during 96 hours and GII) Control group (CTL): animals without deprivation, however kept in individual cages during 96 hours. After this period, the animals of both groups (PSD and CTL) were treated with PILO (i.p., 360mg/kg) to induce limbic seizures. The following parameters were evaluated: A) Number of animals (NA) that presented status epilepticus (SE); B) Sensitivity to PILO after PSD, evaluated by the mortality at the beginning of SE (B1) and 10 days after SE (B10). Sixty days after the induction of SE (second phase of this experiment), both CTL (N=3) and PSD (N=3) groups were submitted to quantitative analysis of neurons undergoing degeneration (Fluoro-Jade B) and expressing potential neuroprotective protein (calretinin) in the hippocampal area. These data were analyzed by means of ANOVA with the post hoc Tukey test. In all statistics tests, a level of significance of p<0.05 was adopted. Results: The data from the first phase revealed: A) The NA that presented SE was slightly higher in PSD (60%) than CTL (50%) animals; B1) Mortality rate during SE was higher in PSD (50%) than CTL (32%) groups; B10) The CTL group presented greater mortality rate (22%) along the time in comparison with the PSD group (7.14%). In the second phase, epileptic animals showed the following findings: The PSD group presented a significant reduction (p=0.02) of degenerating neurons in dentate gyrus, when compared to CTL animals. In addition, the analysis between groups revealed in the PSD group a significant reduction of cells labeled for calretinin (p<0.01) in the dentate gyrus. Conclusions: The above results suggest that rats submitted to the PSD are more susceptible to SE and mortality in the acute phase; however, during the days after SE, the behavioral analysis suggests a protective effect of PSD on the mortality. This fact was strengthened by the reduction of neurodegeneration in epileptic animals of the PSD group, although the expression of the calcium binding proteins analyzed exhibited a decrease in the PSD group. These findings suggest a protective effect of PSD, which cannot be attributable to increased calcium- binding neuroprotection. Other experiments are underway to clarify this phenomenon. Financial Supports: CAPES, FAPESP, FFM-HC, FMUSP (Brazil).