Abstracts

Heat shock protein 70 (HSP70) is a stress inducible protein. In animal models of epilepsy, increased HSP70 expression is proportional to seizure severity. HSP70 neuroprotective mechanisms are not yet elucidated, but HSP70 can attenuate intracellular calcium influx and diminish seizure-induced apoptosis. HSP90 has received little attention in epilepsy research. HSP90 interacts with calcium and calmodulin, and regulates nitric oxide synthase, proteasome, Tau, actine and tubulin, among others. There are few studies about the role of HSP70 in epilepsy and so far nothing regarding to HSP90. Due to the probable HSP70 protective role and the HSP90 relation with key-factor proteins in epileptogenesis, we looked at HSP70 and HSP90 immunohistochemical expression in temporal lobe epilepsy (TLE)., 47 hippocampi were obtained from medically intractable TLE patients: 16 TLE, 18 TLE+depression and 13 TLE+psychosis. 6 control hippocampi were from necropsy cases without past history of neurological disorders, with [italic]pos-mortem[/italic] delay no longer than 4 hours. Specimens were equally treated and submitted to imunohistochemistry to HSP70 and HSP90. Hippocampal regions examined were fascia dentata, hilum, CA4, CA3, CA2, CA1, prosubiculum, subiculum, parahippocampal gyrus and entorhinal cortex. Positive immunoreactivity ([italic]puncta[/italic]) was estimated using the software ImageJ., Analyzes of variancy (ANOVA) of our results showed significant differences. Dunn[apos]s post-hoc tests (p[lt]0.05) of our ANOVA showed significant lower expression of HSP70 and HSP90 in epileptic patients when compared to controls in all hippocampal regions, except fascia dentata and subiculum. Regarding HSP70, the same occurred in all subicular subfields. As to HSP90, there are also differences between TLE+depression and TLE+psychosis at hilum, prosubiculum and hippocampal gyrus. TLE+psychosis always showed values closed to controls., Unlike the reports in animal models the present results indicate that chronic seizures in TLE patients are not sufficient to induce HSP70 and HSP90 activation. Neuronal loss, gliosis and synaptic reorganization, which are typical attributes of TLE, may be determinants of low HSP expression. Inherent to our findings and conclusions, it is important to notice methodological differences between experimental and control groups. Although an effort was made to include only necropsy patients with short post mortem delay, the cause of patients death could be, at least partially, responsible to some degree of HSP activation. Nevertheless, the neurological complications on this group led us to suggest that low expression of HSPs in epileptic groups is related to seizure maintenance. We found no explanation for the differential HSP90 expression in TLE patients with psychosis., (Supported by Fapesp (CInAPCe project # 05/56447-7), CNPq and FAEPA.)