Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity

Zarubenko, I. I.; Yakovlev, A. A.; Stepanichev, M. Yu.; Gulyaeva, N. V.

doi:10.1007/s11055-005-0115-0

Cited by 17 publications

(10 citation statements)

References 45 publications

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“…Naïve bone marrow-injected animals composed, together with medium-injected animals, the control group for the Iba1 quantification (CTRL). Differences between the groups were detected for three main regions of interest, Cx, Hp and SN based on evidence that these areas are involved in motor activity [25] and electroconvulsive seizure susceptibility [26-28]. …”

Section: Resultsmentioning

confidence: 99%

“…Although the tonic component of seizure was protected in MES-BM animals, the stimulated groups (MES-S, MES-DC and MES-BM) presented clonic seizures, which may explain the absence of differences in these areas and consequently suggest their responsiveness to the clonic seizure. In the hippocampus, a structure that is susceptible to convulsive seizures [42,43], and that contains cells vulnerable to electroshock [26-28], transplantation of bone marrow cells in MES animals was able to raise the number of microglial cells. Concerning these data, we speculated whether the observed increase in Iba1 cells in the hippocampus was due to its role in generalized or focal seizures and/or by a direct participation on persisting clonic seizures.…”

Section: Discussionmentioning

confidence: 99%

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Anticonvulsant activity of bone marrow cells in electroconvulsive seizures in mice

et al. 2013

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BackgroundBone marrow is an accessible source of progenitor cells, which have been investigated as treatment for neurological diseases in a number of clinical trials. Here we evaluated the potential benefit of bone marrow cells in protecting against convulsive seizures induced by maximum electroconvulsive shock (MES), a widely used model for screening of anti-epileptic drugs. Behavioral and inflammatory responses were measured after MES induction in order to verify the effects promoted by transplantation of bone marrow cells. To assess the anticonvulsant effects of bone marrow cell transplantation, we measured the frequency and duration of tonic seizure, the mortality rate, the microglial expression and the blood levels of cytokine IL-1, IL-6, IL-10 and TNF-α after MES induction. We hypothesized that these behavioral and inflammatory responses to a strong stimulus such as a convulsive seizure could be modified by the transplantation of bone marrow cells.ResultsBone marrow transplanted cells altered the convulsive threshold and showed anticonvulsant effect by protecting from tonic seizures. Bone marrow cells modified the microglial expression in the analyzed brain areas, increased the IL-10 and attenuate IL-6 levels.ConclusionsBone marrow cells exert protective effects by blocking the course of electroconvulsive seizures. Additionally, electroconvulsive seizures induced acute inflammatory responses by altering the pattern of microglia expression, as well as in IL-6 and IL-10 levels. Our findings also indicated that the anticonvulsant effects of these cells can be tested with the MES model following the same paradigm used for drug testing in pharmacological screening. Studies on the inflammatory reaction in response to acute seizures in the presence of transplanted bone marrow cells might open a wide range of discussions on the mechanisms relevant to the pathophysiology of epilepsies.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anticonvulsant activity of bone marrow cells in electroconvulsive seizures in mice

et al. 2013

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“…Zarubenko et al [75] have shown that repeated ECS causes neuronal death. On the other hand, a number of studies have shown that repeated ECS increases neurogenesis [76–78].…”

Section: Discussionmentioning

confidence: 99%

Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat

Limoa

Hashioka

Miyaoka

et al. 2016

J Neuroinflammation

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BackgroundAlthough electroconvulsive therapy (ECT) is regarded as one of the efficient treatments for intractable psychiatric disorders, the mechanism of therapeutic action remains unclear. Recently, many studies indicate that ECT affects the immune-related cells, such as microglia, astrocytes, and lymphocytes. Moreover, microglial activation and astrocytic activation have been implicated in the postmortem brains of schizophrenia patients. We previously demonstrated that Gunn rats showed schizophrenia-like behavior and microglial activation in their brains. The present study examined the effects of electroconvulsive shock (ECS), an animal counterpart of ECT, on schizophrenia-like behavior, microgliosis, and astrogliosis in the brain of Gunn rats.MethodsThe rats were divided into four groups, i.e., Wistar sham, Wistar ECS, Gunn sham, and Gunn ECS. ECS groups received ECS once daily for six consecutive days. Subsequently, prepulse inhibition (PPI) test was performed, and immunohistochemistry analysis was carried out to determine the activation degree of microglia and astrocytes in the hippocampus by using anti-CD11b and anti-glial fibrillary acidic protein (GFAP) antibody, respectively.ResultsWe found PPI deficit in Gunn rats compared to Wistar rats, and it was significantly improved by ECS. Immunohistochemistry analysis revealed that immunoreactivity of CD11b and GFAP was significantly increased in Gunn rats compared to Wistar rats. ECS significantly attenuated the immunoreactivity of both CD11b and GFAP in Gunn rats.ConclusionsECS ameliorated schizophrenia-like behavior of Gunn rats and attenuated microgliosis and astrogliosis in the hippocampus of Gunn rats. Accordingly, therapeutic effects of ECT may be exerted, at least in part, by inhibition of glial activation. These results may provide crucial information to elucidate the role of activated glia in the pathogenesis of schizophrenia and to determine whether future therapeutic interventions should attempt to up-regulate or down-regulate glial functions.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-016-0688-2) contains supplementary material, which is available to authorized users.

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“…Like ECS, pilocarpine‐induced status epilepticus also causes dramatic and prolonged increases in cell proliferation in the SGZ (Gray and Sundstrom,1998; Parent et al,1997). However, prolonged seizures can thus cause synaptic reorganization with sprouting, involving aberrant growth of neural networks including granular cell axons (so‐called mossy fibers) in the SGZ of the fascia dentate and sprouting of CA1 axons in the CA1 subfield (Gombos et al,1999; Smith and Dudek,2001; Zarubenko et al,2005; Zhang et al,1998). Antidepressant drugs also increase cell proliferation in the dentate gyrus (Malberg et al,2000).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, apoptotic cells increased only 10‐fold in the ECS groups. Prolonged continuous seizure activity, as seen in status epilepticus, triggers neuronal cell death in the brain regions through which the seizure propagates (Zarubenko et al,2005; Zhang et al,1998). No significant increase in apoptotic cells was observed after 20 ECSs in our study, whereas apoptosis may be induced following prolonged continuous seizure.…”

Section: Discussionmentioning

confidence: 99%

Effects of repeated electroconvulsive seizure on cell proliferation in the rat hippocampus

Ito

Seki

Liu

et al. 2010

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Electroconvulsive therapy (ECT) is known as a successful treatment for severe depression. Despite great efforts, the biological mechanisms underlying the beneficial effects of ECT remain largely unclear. In this study, animals received a single, 10, or 20 applications of electroconvulsive seizure (ECS), and then cell proliferation and apoptosis were investigated in the subgranular zone (SGZ) of the dentate gyrus. We analyzed whether a series of ECSs could induce changes in the dentate gyrus in a dose-response fashion. A single-ECS seizure significantly increased cell proliferation in the SGZ by ∼2.3-fold compared to sham treatment. After 10 ECSs, a significant increase in cell proliferation was observed in the SGZ by ∼2.4-fold compared to sham treatment. Moreover, 10 ECSs induced a significant increase in cell proliferation by 1.3-fold compared to a single-ECS group. However, cell proliferation did not differ between the group with 20 ECSs and sham group. In addition, a significant increase in the number of apoptotic cells was found in the group with 10 ECSs, whereas no significant change in it was found in either a single ECS or 20 ECSs group compared to sham treatment. These findings indicate that the optimal number of treatments and duration of stimulation requires investigation. Further studies are needed to elucidate the intracellular mechanisms underlying both effective and excessive ECT.

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Electroconvulsive Shock Induces Neuron Death in the Mouse Hippocampus: Correlation of Neurodegeneration with Convulsive Activity

Cited by 17 publications

References 45 publications

Anticonvulsant activity of bone marrow cells in electroconvulsive seizures in mice

Anticonvulsant activity of bone marrow cells in electroconvulsive seizures in mice

Electroconvulsive shock attenuated microgliosis and astrogliosis in the hippocampus and ameliorated schizophrenia-like behavior of Gunn rat

Effects of repeated electroconvulsive seizure on cell proliferation in the rat hippocampus

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