Researchers from the Karolinska Institute in Sweden have just published an article about the effect of ECT on rats.*
The article begins:
“Electroconvulsive therapy (ECT) is used to treat patients with major depressive disorder who do not respond to pharmacologic treatment. However, the treatment does not only attenuate symptoms of depression, it can also cause long lasting memory deficits.”
It is unusual to see such a straightforward description in the scientific literature of memory loss caused by ECT. Usually any mention of memory loss is qualified by words such as rare, mostly transient, mild, etc.
The article concludes:
“Rats subjected to a single ECS event demonstrate a complex, transient regulation of levels of Nogo receptors, BDNF and AMPA receptors in the dentate gyrus and other parts of the hippocampal formation. It is suggested that these events are temporally and spatially orchestrated to open a time window permissive to synaptic plasticity, followed by closure of this window, leading to a lasting alteration of synaptic circuitry. This could underlie both the beneficial antidepressant effects and the amnesic side effects of ECT treatment.”
Earlier this year Frontiers in Psychiatry published an article, Electroconvulsive treatment: hypotheses about mechanisms of action, by John Read of Liverpool University and Roar Fosse from the Vestre Viken State Hospital Trust, Lier, Norway.** The authors reviewed the literature and concluded:
“We suggest that the temporarily improved scores on depression instruments following ECT reflect the combination of frontal and temporal lobe functional impairments and activation of the HPA axis and the mesocorticolimbic dopamine system. These effects as well as other detailed changes observed in structures such as the hippocampus appear consistent with those typically seen after severe stress-exposure and/or brain trauma. Hence, we conjecture that central to the effect mechanisms of ECT is the impact upon the brain in a manner that is consistent with a unique type of severe stress-exposure or trauma.”
I am not sure how the Swedish researchers’ “window permissive of synaptic plasticity” relates to the conclusion of the authors of the second article, but it is interesting to see two articles published recently which have both taken memory loss into consideration when attempting to find a possible mechanism of action for ECT.
* Nordgren M, Karlsson T, Svensson M, Koczy J, Josephson A, et al. (2013) Orchestrated Regulation of Nogo Receptors, Lotus, AMPA Receptors and BDNF in an ECT Model Suggests Opening and Closure of a Window of Synaptic Plasticity. PLoS ONE 8(11): e78778. doi:10.1371/journal.pone.0078778
** Fosse R and Read J (2013) Electroconvulsive treatment: hypotheses about mechanisms of action. Front. Psychiatry 4:94. doi: 10.3389/fpsyt.2013.00094