Electroconvulsive seizure-induced changes in gene expression in the mouse hypothalamic paraventricular nucleus

Sakaida, Mari; Sukeno, Mamiko; Imoto, Yuki; Tsuchiya, Soken; Sugimoto, Yukihiko; Okuno, Yasushi; Segi-Nishida, Eri

doi:10.1177/0269881113497612

Cited by 15 publications

(14 citation statements)

References 26 publications

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“…An electrical current of 80 mC (80 mA, 50 Hz, 1s duration and 0.5 ms pulse width) generated by an ECT unit (Ugo Basile, Italy) was applied via ear clip electrodes. This current induced a tonic-clonic seizure lasting 5–20 seconds, with an overall average seizure duration (± SD) of 13.0 ± 2.2 seconds (12.9 ± 2.2 for the control group and 13.1 ± 2.2 for the CSS group) Averages of individual mice over all 10 ECS sessions ranged from 11.1 to 14.5 seconds, which was comparable to seizure duration induced by ECS in other studies [ 42 , 44 , 45 ]. The other half of the mice underwent a sham procedure comprising anaesthesia, ear cleaning and electrode attachment in the absence of ECS.…”

Section: Methodssupporting

confidence: 76%

Mouse repeated electroconvulsive seizure (ECS) does not reverse social stress effects but does induce behavioral and hippocampal changes relevant to electroconvulsive therapy (ECT) side-effects in the treatment of depression

et al. 2017

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Electroconvulsive therapy (ECT) is an effective treatment for depression, but can have negative side effects including amnesia. The mechanisms of action underlying both the antidepressant and side effects of ECT are not well understood. An equivalent manipulation that is conducted in experimental animals is electroconvulsive seizure (ECS). Rodent studies have provided valuable insights into potential mechanisms underlying the antidepressant and side effects of ECT. However, relatively few studies have investigated the effects of ECS in animal models with a depression-relevant manipulation such as chronic stress. In the present study, mice were first exposed to chronic social stress (CSS) or a control procedure for 15 days followed by ECS or a sham procedure for 10 days. Behavioral effects were investigated using an auditory fear conditioning (learning) and expression (memory) test and a treadmill-running fatigue test. Thereafter, immunohistochemistry was conducted on brain material using the microglial marker Iba-1 and the cholinergic fibre marker ChAT. CSS did not increase fear learning and memory in the present experimental design; in both the control and CSS mice ECS reduced fear learning and fear memory expression. CSS induced the expected fatigue-like effect in the treadmill-running test; ECS induced increased fatigue in CSS and control mice. In CSS and control mice ECS induced inflammation in hippocampus in terms of increased expression of Iba-1 in radiatum of CA1 and CA3. CSS and ECS both reduced acetylcholine function in hippocampus as indicated by decreased expression of ChAT in several hippocampal sub-regions. Therefore, CSS increased fatigue and reduced hippocampal ChAT activity and, rather than reversing these effects, a repeated ECS regimen resulted in impaired fear learning-memory, increased fatigue, increased hippocampal Iba-1 expression, and decreased hippocampal ChAT expression. As such, the current model does not provide insights into the mechanism of ECT antidepressant function but does provide evidence for pathophysiological mechanisms that might contribute to important ECT side-effects.

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Section: Methodssupporting

confidence: 76%

Mouse repeated electroconvulsive seizure (ECS) does not reverse social stress effects but does induce behavioral and hippocampal changes relevant to electroconvulsive therapy (ECT) side-effects in the treatment of depression

et al. 2017

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“…Mice were anesthetized with sevoflurane, and electroconvulsive shocks were delivered via ear clip electrodes using a pulse generator (Ugo Basile, Comerio, Italy), set at the following shock parameters: 80 mA, 50 Hz, 1 s duration, and 0.5 ms pulse width. All mice developed tonic-clonic seizures lasting approximately 10–15 s, which is comparable to the seizure duration induced by electroconvulsive seizures (ECS) in other experiments [ 28 – 30 ]. The total duration of anesthesia was approximately 5 min per mouse.…”

Section: Methodssupporting

confidence: 75%

Electroconvulsive seizures (ECS) do not prevent LPS-induced behavioral alterations and microglial activation

Buel

Bosker

Drunen

et al. 2015

J Neuroinflammation

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BackgroundLong-term neuroimmune activation is a common finding in major depressive disorder (MDD). Literature suggests a dual effect of electroconvulsive therapy (ECT), a highly effective treatment strategy for MDD, on neuroimmune parameters: while ECT acutely increases inflammatory parameters, such as serum levels of pro-inflammatory cytokines, there is evidence to suggest that repeated ECT sessions eventually result in downregulation of the inflammatory response. We hypothesized that this might be due to ECT-induced attenuation of microglial activity upon inflammatory stimuli in the brain.MethodsAdult male C57Bl/6J mice received a series of ten electroconvulsive seizures (ECS) or sham shocks, followed by an intracerebroventricular (i.c.v.) lipopolysaccharide (LPS) or phosphate-buffered saline (PBS) injection. Brains were extracted and immunohistochemically stained for the microglial marker ionized calcium-binding adaptor molecule 1 (Iba1). In addition, a sucrose preference test and an open-field test were performed to quantify behavioral alterations.ResultsLPS induced a short-term reduction in sucrose preference, which normalized within 3 days. In addition, LPS reduced the distance walked in the open field and induced alterations in grooming and rearing behavior. ECS did not affect any of these parameters. Phenotypical analysis of microglia demonstrated an LPS-induced increase in microglial activity ranging from 84 to 213 % in different hippocampal regions (CA3 213 %; CA1 84 %; dentate gyrus 131 %; and hilus 123 %). ECS-induced alterations in microglial activity were insignificant, ranging from −2.6 to 14.3 % in PBS-injected mice and from −20.2 to 6.6 % in LPS-injected mice.ConclusionsWe were unable to demonstrate an effect of ECS on LPS-induced microglial activity or behavioral alterations.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-015-0454-x) contains supplementary material, which is available to authorized users.

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“… a Sources: (Ravizza et al, 2001), b (Tang et al, 2002), c (Elliott et al, 2003), d (Wilson et al, 2005), e (Okamoto et al, 2010), f (Sakaida et al, 2013), g (Almeida-Suhett et al, 2014), h (Samal et al, 2015), i (Zamanian et al, 2012), j (Zhang et al, 2016), k (Rakhade et al, 2005), l (Boer et al, 2010), m (Beaumont et al, 2012) …”

Section: Figmentioning

confidence: 99%

Altered gene expression profile in a mouse model of SCN8A encephalopathy

Sprissler

Wagnon

Bunton-Stasyshyn

et al. 2017

Experimental Neurology

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SCN8A encephalopathy is a severe, early-onset epilepsy disorder resulting from de novo gain-of-function mutations in the voltage-gated sodium channel Nav1.6. To identify the effects of this disorder on mRNA expression, RNA-seq was performed on brain tissue from a knock-in mouse expressing the patient mutation p.Asn1768Asp (N1768D). RNA was isolated from forebrain, cerebellum, and brainstem both before and after seizure onset, and from age-matched wildtype littermates. Altered transcript profiles were observed only in forebrain and only after seizures. The abundance of 50 transcripts increased more than 3-fold and 15 transcripts decreased more than 3-fold after seizures. The elevated transcripts included two anti-convulsant neuropeptides and more than a dozen genes involved in reactive astrocytosis and response to neuronal damage. There was no change in the level of transcripts encoding other voltage-gated sodium, potassium or calcium channels. Reactive astrocytosis was observed in the hippocampus of mutant mice after seizures. There is considerable overlap between the genes affected in this genetic model of epilepsy and those altered by chemically induced seizures, traumatic brain injury, ischemia, and inflammation. The data support the view that gain-of-function mutations of SCN8A lead to pathogenic alterations in brain function contributing to encephalopathy.

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Electroconvulsive seizure-induced changes in gene expression in the mouse hypothalamic paraventricular nucleus

Cited by 15 publications

References 26 publications

Mouse repeated electroconvulsive seizure (ECS) does not reverse social stress effects but does induce behavioral and hippocampal changes relevant to electroconvulsive therapy (ECT) side-effects in the treatment of depression

Mouse repeated electroconvulsive seizure (ECS) does not reverse social stress effects but does induce behavioral and hippocampal changes relevant to electroconvulsive therapy (ECT) side-effects in the treatment of depression

Electroconvulsive seizures (ECS) do not prevent LPS-induced behavioral alterations and microglial activation

Altered gene expression profile in a mouse model of SCN8A encephalopathy

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