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

Abstract

Electroconvulsive therapy is an effective and rapid treatment for depression. In patients with depression, the function of the paraventricular nucleus of the hypothalamus (PVN) is frequently altered. Electroconvulsive seizure (ECS), which is a model of electroconvulsive therapy, upregulates the expression of c-fos in the PVN of animal models. Therefore, we hypothesized that ECS alters gene expression and function in the PVN. The PVN was microdissected from mouse brain sections following ECS treatment, and total RNA was analyzed by microarray. Two hours after ECS, the levels of expression of 2.6% (589 genes) of the genes showed a greater than 2-fold decrease and 0.9% (205 genes) showed a greater than 2-fold increase. Among these genes, 72 of the downregulated genes and 12 of the upregulated genes have been proposed to be associated with psychiatric disorders, such as depression, by knowledge database analyses. The groups of downregulated genes included neuropeptides (Cck), kinases (Prkcb, Camk2a), transcription factors (Tcf4), and transporters (Aqp4), and these have been suggested to be associated with psychiatric disorders and/or PVN function. The results of the present study indicated that ECS treatment could modulate PVN functions through altered gene expression, which may contribute to its antidepressant effects.

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

“…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.…”

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

“…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.…”

Altered gene expression profile in a mouse model of SCN8A encephalopathy

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