Elektrokonvulzı̇f Nöbetlerı̇n Farelerde Nöroı̇nflamatuvar Yanıt Üzerı̇ndekı̇ Olası Etkı̇sı̇ ve Bu Etkı̇nı̇n Doğurduğu Sonuçların İncelenmesı̇

Abstract

Neuroinflammation has been shown to be involved in pathological conditions like cortical spreading depression, seizures and ischemia. Its involvement in physiological processes like neurogenesis, learning and memory has also been reported. Recent research also points out a role for neuroinflammation in intercellular signaling in the central nervous system, which is triggered by homeostatic imbalance. Based on these findings, we hypothesized that neuroinflammation may have a central role in understanding mechanisms of action of electroconvulsive therapy (ECT), one of the oldest and most effective treatments in psychiatry. Limited data points to a microglial activation after ECT, but to our knowledge, the neuroinflammatory response originating from neurons and other glial cells after ECT has not been examined before. In our study, we aimed to focus on neuroinflammatory response after a single electroconvulsive seizure (ECS), which is a rodent model of ECT. We examined expression and secretion of HMGB1, which is known to have a proinflammatory role outside the cell, at four time points after a single ECS (1, 2 , 4 and 6 hours). We detected a lower ratio of HMGB1 (+) cell compared to sham group in the hippocampus and medial regions of frontal cortex by immunohistochemical staining and increased amount of HMGB1 level in cerebrospinal fluid. There were no differences in HMGB protein expression in hippocampus and prefrontal cortex between sham operated animals and ECS group as detected by Western blotting. Moreover, brain derived neurotropic factor (BDNF) level was increased in hippocampus and prefrontal cortex 1 hour and 6 hours after ECT, respectively. These findings may suggest a relationship between the HMGB1 release and BDNF increase but this hypothesis remains to be tested.