Electroconvulsive therapy in melancholia: the role of hippocampal neurogenesis

To elucidate the relationship between the effects of electroconvulsive therapy (ECT) on hippocampal anatomy and function in the therapy of melancholic depression and preclinical observations of increased neurogenesis in the hippocampus of experimental animals receiving electroconvulsive seizures (ECS). We emphasize the role of hypercortisolaemia in melancholic depression and in experimental hippocampal neurogenesis.

Our statements are based on a variety of studies pointing to i) ECT being superior to all other treatment modalities in the therapy of melancholia, ii) melancholia being associated with hypercortisolaemia and iii) evidence of hippocampal neurogenesis being relevant for understanding both melancholia and ECT.

The increased neurogenesis found in animal studies shows stronger effect of seizures than of antidepressant drugs. The onset of effect is not only faster but is also sustained. Newborn cells are found to be functional. Suppression of neurogenesis by chronic treatment with corticosterone is associated with depression-like biology and behaviour making comparison with human depression and its response to ECT relevant.

We hypothesize that the superior antimelancholic effect of induced seizures may be understood in the light of the powerful control of neural plasticity exerted by the regulation of the hypothalamic-pituitary-adrenal axis and, perhaps, other regulatory factors.