HPA axis normalization, estimated by DEX/CRH test, but less alteration on cerebral glucose metabolism in depressed patients receiving ECT after medication treatment failures

Yuuki, Naoya; Ida, Iturou; Oshima, Akihiro; Kumano, Hiroshi; Takahashi, Keisuke; Fukuda, Masato; Oriuchi, Noboru; Endo, Keigo; Matsuda, Hiroshi; Murakami, Masahiko

doi:10.1111/j.1600-0447.2005.00625.x

Cited by 61 publications

(29 citation statements)

References 34 publications

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“…brain regions (Prohovnik et al, 1986;Rosenberg et al, 1988;Scott et al, 1994;Silfverskiöld et al, 1986). Studies that measured the long-term effects of ECT also found a decrease in CBF or glucose metabolism in the frontal, parietal, and temporal lobes (Henry et al, 2001;Nobler et al, 2001;Yuuki et al, 2005;Suwa et al, 2012). Three studies reported an increase in regional blood flow in similar cortical regions (Bonne et al, 1996;Mervaala et al, 2001;Suwa et al, 2012).…”

Section: Discussionmentioning

confidence: 92%

Effect of electroconvulsive therapy on gray matter volume in major depressive disorder

Ota

Noda

Sato

et al. 2015

Journal of Affective Disorders

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Section: Discussionmentioning

confidence: 92%

Effect of electroconvulsive therapy on gray matter volume in major depressive disorder

Ota

Noda

Sato

et al. 2015

Journal of Affective Disorders

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“…In this way, SPECT and PET studies on the effects of ECT on brain activities in depressed patients have led to conflicting results, ranging from overall decrease [18][19][20] to increase [21]. In addition, Yuuki et al [22] demonstrated hypometabolism in some parts of prefrontal regions and hypermetabolism in the parietal and occipital lobes after ECT treatment. In addition, several genes involved in the metabolic regulation are up-regulated chronically after ECS, mainly in the hippocampus [12].…”

Section: Tbars Acutementioning

confidence: 96%

Long Lasting Effects of Electroconvulsive Seizures on Brain Oxidative Parameters

et al. 2006

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This work was performed in order to determine the level of oxidative damage and antioxidant enzymes activities late after acute and chronic electroconvulsive shock (ECS) in rats. We measured oxidative parameters in hippocampus, cortex, and striatum, at 45, 60, 90 and 120 days after a single or multiple ECS. We demonstrated an increase in lipid peroxidation after multiple ECS in the hippocampus and striatum. This was also the case for protein carbonyls in the single or multiple protocols. In this way, we demonstrated an increase in catalase in cortex in contrast to striatum and hippocampus, were there were decreases sometimes in chronic ECS. The superoxide dismutase activities decrease in different times after single and multiple ECS in the hippocampus. Our findings demonstrated that there is a delayed increase after ECS in oxidative damage and decrease in antioxidant enzymes activities in hippocampus and striatum.

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“…Successful ECT treatment is associated with normalization of hypothalamic-pituitary-adrenal (HPA) axis abnormalities in this patient population [3, 4]. The hippocampus is a limbic brain region that is particularly sensitive to excitotoxic insults that arise from elevated levels of circulating glucocorticoids, and it plays a key role in the stress response by providing negative feedback inhibition over the HPA axis[5-7].…”

Section: Introductionmentioning

confidence: 99%

Antidepressant-like Effects of Electroconvulsive Seizures Require Adult Neurogenesis in a Neuroendocrine Model of Depression

et al. 2015

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Background Neurogenesis continues throughout life in the hippocampal dentate gyrus. Chronic treatment with monoaminergic antidepressant drugs stimulates hippocampal neurogenesis, and new neurons are required for some antidepressant-like behaviors. Electroconvulsive seizures (ECS), a laboratory model of electroconvulsive therapy (ECT), robustly stimulate hippocampal neurogenesis. Hypothesis ECS requires newborn neurons to improve behavioral deficits in a mouse neuroendocrine model of depression. Methods We utilized immunohistochemistry for doublecortin (DCX), a marker of migrating neuroblasts, to assess the impact of Sham or ECS treatments (1 treatment per day, 7 treatments over 15 days) on hippocampal neurogenesis in animals receiving 6 weeks of either vehicle or chronic corticosterone (CORT) treatment in the drinking water. We conducted tests of anxiety- and depressive-like behavior to investigate the ability of ECS to reverse CORT-induced behavioral deficits. We also determined whether adult neurons are required for the effects of ECS. For these studies we utilized a pharmacogenetic model (hGFAPtk) to conditionally ablate adult born neurons. We then evaluated behavioral indices of depression after Sham or ECS treatments in CORT-treated wild-type animals and CORT-treated animals lacking neurogenesis. Results ECS is able to rescue CORT-induced behavioral deficits in indices of anxiety- and depressive-like behavior. ECS increases both the number and dendritic complexity of adult-born migrating neuroblasts. The ability of ECS to promote antidepressant-like behavior is blocked in mice lacking adult neurogenesis. Conclusion ECS ameliorates a number of anxiety- and depressive-like behaviors caused by chronic exposure to CORT. ECS requires intact hippocampal neurogenesis for its efficacy in these behavioral indices.

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HPA axis normalization, estimated by DEX/CRH test, but less alteration on cerebral glucose metabolism in depressed patients receiving ECT after medication treatment failures

Abstract: Depressed patients who failed trials of antidepressant medication showed a remission with ECT that was accompanied by resolution of HPA dysregulation. However, measures of cerebral brain metabolism did not resolve.

Cited by 61 publications

References 34 publications

Effect of electroconvulsive therapy on gray matter volume in major depressive disorder

Effect of electroconvulsive therapy on gray matter volume in major depressive disorder

Long Lasting Effects of Electroconvulsive Seizures on Brain Oxidative Parameters

Antidepressant-like Effects of Electroconvulsive Seizures Require Adult Neurogenesis in a Neuroendocrine Model of Depression

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