Abstract
Electroconvulsive therapy (ECT) is an efficient and relatively fast acting treatment for depression. However, one severe side effect of the treatment is retrograde amnesia, which in certain cases can be long-term. The mechanisms behind the antidepressant effect and the amnesia are not well understood. We hypothesized that ECT causes transient downregulation of key molecules needed to stabilize synaptic structure and to prevent Ca2+ influx, and a simultaneous increase in neurotrophic factors, thus providing a short time window of increased structural synaptic plasticity. Here we followed regulation of NgR1, NgR3, LOTUS, BDNF, and AMPA subunits GluR1 and GluR2 flip and flop mRNA levels in hippocampus at 2, 4, 12, 24, and 72 hours after a single episode of induced electroconvulsive seizures (ECS) in rats. NgR1 and LOTUS mRNA levels were transiently downregulated in the dentate gyrus 2, 4, 12 and 4, 12, 24 h after ECS treatment, respectively. GluR2 flip, flop and GluR1 flop were downregulated at 4 h. GluR2 flip remained downregulated at 12 h. In contrast, BDNF, NgR3 and GluR1 flip mRNA levels were upregulated. Thus, ECS treatment induces a transient regulation of factors important for neuronal plasticity. Our data provide correlations between ECS treatment and molecular events compatible with the hypothesis that both effects and side effects of ECT may be caused by structural synaptic rearrangements.
Highlights
Electroconvulsive therapy (ECT) is used to treat patients with major depressive disorder who do not respond to pharmacologic treatment
Nogo receptor 1 (NgR1) mRNA levels had returned to sham levels 24 hours after electroconvulsive seizures (ECS)
NgR3 mRNA expression The expression of NgR3 increased in all brain areas analyzed following ECS compared with sham, but was most marked in the dentate gyrus (Fig. 1 and 2) where levels were significantly higher at 2 (p,0.01) and 4 h (p,0.001) before returning to baseline levels
Summary
Electroconvulsive therapy (ECT) is used to treat patients with major depressive disorder who do not respond to pharmacologic treatment. The treatment does attenuate symptoms of depression, it can cause long lasting memory deficits Both the amnesia and the superiority of ECT over antidepressant drugs is well-established [1], but the underlying mechanisms of action are still largely unknown. Robust effects on regulation of levels of signaling molecules and trophic factors have been revealed in rats in response to electroconvulsive seizures (ECS), used to model ECT [2]. Many of these effects were observed in hippocampus, an important region for learning and memory [3]. Treatment with ECS increases BDNF protein and mRNA in hippocampus of rat [2,5,6]
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