Chronic electroconvulsive shock and neurotransmitter receptors - An update -

Gleiter, Christoph H.; Nutt, David

doi:10.1016/0024-3205(89)90550-x

Cited by 58 publications

(21 citation statements)

References 124 publications

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“…The receptor hypothesis emphasizes alterations in neurotransmitter receptors as the primary mechanism of action of ECS in affective disorders (30)(31)(32)(33). This hypothesis invokes common mechanisms in mediating the therapeutic effects of ECS and antidepressant drugs but does not account for the finding that some depressed patients respond to ECS but not to drugs (34).…”

Section: Discussionmentioning

confidence: 99%

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Brady

Lynn²,

Glowa³

et al. 1994

J. Clin. Invest.

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Electroconvulsive shock (ECS) is a highly effective therapy for the treatment of major depression, but its mechanisms of action are not known. We report that repeated ECS in rats produces enduring changes in two clinically relevant stress-responsive brain systems: (a) the hypothalamic-pituitary-adrenal axis regulated by corticotropin-releasing hormone (CRH) in the paraventricular nucleus; and (b) the NE system in the locus coeruleus regulated by tyrosine hydroxylase (TH). CRH and TH mRNA levels in these brain regions were assessed by in situ hybridization histochemistry. A single interaural ECS elevated TH but not CRH mRNA measured 24 h later. Repeated daily treatments (3, 7, or 14) elevated both mRNAs, maximally with 7, correlating with the time course of clinical efficacy. The elevations persisted for 3 (CRH) or 8 wk (TH) after the ECS. No other therapeutic treatment is known to produce such longlasting changes in central nervous system gene expression. The time course of events (delayed onset, long duration) implicate CRH as a principal mediator of the antidepressant effects of ECS. The locus coeruleus-NE system may be important in initiating the central nervous system response. (J. Clin. Invest. 1994.94:1263-1268

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Section: Discussionmentioning

confidence: 99%

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Brady

Lynn²,

Glowa³

et al. 1994

J. Clin. Invest.

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“…A chronic increase of mediator concentration in the extracellular space could also have other effects on receptor function including various forms of desensitization: receptor uncoupling, receptor affinity changes, and down-regulation of receptor number (Sibley & Lefkowitz, 1985). The advent of a selective receptor ligand has allowed direct assessment of ECS-evoked D1 receptor changes in the caudate nucleus and a decrease in agonist binding by 35 % has been reported (Gleiter & Nutt, 1989). Many other factors may also make substantial contributions to the effects of ECS, such as changes in the activity of voltage controlled ion channels produced by a direct effect of transmitters (Nicoll, 1982), and modulatory interactions of different neurotransmitters in the striatum (Racagni, Bruno, Cattabeni, Maggi, DiGiulio & Groppetti, 1978) which are released concomitantly by ECS.…”

Section: Discussionmentioning

confidence: 99%

“…Chronic ECS has a number of reproducible actions on brain neurotransmitters and their receptors. Many of these changes (specific in action and having clear regional differences) can plausibly be linked to positive behavioural alterations in psychopathic patients (Gleiter & Nutt, 1989).…”

Section: Discussionmentioning

confidence: 99%

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Catecholamine overflow within rat striatum: the influence of microstimulation and electroconvulsive stimulation as observed with voltammetry

Pavlásek¹,

Masánová²,

Haburčák³

et al. 1994

Experimental Physiology

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SUMMARYDifferential pulse voltammetry with a carbon fibre microelectrode was used in chloral hydrateanaesthetized rats for testing the influence of microstimulation and of electroconvulsive stimulation on the changes in concentration of electro-oxidizable materials (catechol derivates) in the extracellular space of the corpus striatum. Microstimulation applied in the striatum (8 V anodal pulses, 01 ms, 100 Hz for 40 s) caused a significant increase of the catechol-oxidative current (I); 5 s after microstimulation was stopped I'o ranged from I 1 7 to 141 % of the control (all values means + S.D. unless otherwise stated; 124+ II %, n = 4, P < 0-01, Student's t test).This effect ceased in the third minute after microstimulation. A comparable result was observed when microstimulation was repeated at intervals of 10 min. Electroconvulsive stimulation with a sinusoidal current (50 Hz, approximately 150 mA, 0 2 s) caused a large increase in I40; 20 s after stimulation ceased, I,, was 987 + 900% (n = 3) of the control and it returned to the baseline 2 min later. The mechanisms inducing transmitter overflow are considered and the influence of electroconvulsive stimulation on the striatum is discussed in the context of its beneficial effects in psychopathic patients.

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“…In neurotransmitters and their receptors in the brain, ECS produces various changes, many of which can be linked to its therapeutic effect. Chronic ECS application influences 5-hydroxytryptamine (5-HT) 1A receptors, β-adrenoreceptors, α2-adrenoreceptors, adenosine A1 receptors, muscarinic receptors (6) and N-methyl-D-aspartic acid (NMDA) receptor complex (7). ECS also activates cell signaling and leads to release of second messengers (8).…”

Section: Introductionmentioning

confidence: 99%

Depresyonda EKT Sonrası Süperoksit Dismutaz Aktivitesi Düşüyor ve EKT'ye Kötü Yanıtla Korelasyon Gösteriyor

Virit¹,

Dalkılıç²,

Bulut³

et al. 2011

Npa

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ÖZET Amaç:Elektrokonvülzif tedavinin (EKT) oksidatif metabolizma üzerine etkileri ile ilgili literatürün ço¤u hayvan deneylerine dayanmaktad›r ve oksidan/antioksidan dengenin de¤iflti¤ine dair çeliflkili sonuçlar içermektedir. Bu alanda yap›lan ilk insan çal›flmas› olan bu çal›flman›n amac› depresif hastalarda EKT sonras› oksidan ve antioksidanlardaki de¤iflimleri araflt›rmakt›r. Yöntemler: On dört unipolar ve iki bipolar depresyon hastas› çal›flmaya dahil edildi. Kan örnekleri ilk EKT seans›ndan 1 saat once ve 7. EKT seans›ndan 1 saat sonra al›nd›. Plazmada oksidanlardan malondialdehit (MDA), nitrik oksit (NO) ve ksantin oksidaz (XO); antioksidanlardan süperoksit dismutaz (SOD) seviyeleri ölçüldü. Bulgular: Birinci ve 7. EKT seans›ndan sonraki Hamilton Depresyon Ölçe¤i (HAM-D) skorlar› 32.63±9.54 ve 16.50±7.22 idi (t=7.92, df=15, p<0.001). Yedinci EKT sonras› SOD de¤erleri EKT öncesi SOD de¤erlerinden anlaml› olarak düflüktü (p<0.05, Z= -3,459). EKT öncesi ve sonras› MDA, NO ve XO de¤erleri aras›nda anlaml› bir farkl›l›k yoktu (p>0.05). Bununla birlikte, EKT öncesi SOD de¤erleri EKT öncesi HAM-D skorlar› ile anlaml› düzeyde pozitif korelasyon gös-teriyordu (r=0.641, p=0.007). Sonuç: EKT sonras› antioksidan bir enzim olan SOD düzeyindeki düflüfl oksidatif stresi artt›rarak nöronlara zarar verebilir. Bu nedenle EKT uygulama dönemlerinde antioksidan ekleme tedavilerinin olas› faydalar› araflt›r›lmal›d›r. Yine EKT öncesi yüksek oksidan seviyeleri depresyon hastalar›nda EKT'ye kötü yan›t› yordayabilir. (Nöropsikiyatri Arflivi 2010; 47: 247-51) Anahtar kelimeler: Elektrokonvülzif tedavi, Oksidatif metabolizma, Süperoksit dismutaz ABSTRACT Objective: The literature regarding effects of electroconvulsive therapy (ECT) on oxidative metabolism (OM) reports conflicting changes in oxidant and antioxidant status in animal studies. The goal of this first human study was to investigate the changes in oxidants and antioxidants in plasma of depressed patients after ECT. Methods: Fourteen unipolar and two bipolar patients were included in the study. The blood samples were obtained within one hour before the 1 st and within one hour after the 7 th ECT sessions. Oxidants malondialdehyde (MDA), nitric oxide (NO), and xanthine oxidase (XO) and antioxidant superoxide dismutase (SOD) were measured in the plasma. Results: Before the 1 st and after the 7 th ECT sessions, the Hamilton Depression Rating Scale (HDRS) scores were 32.63±9. 54 and 16.50±7.22, respectively (t=7.92, df=15, p<0.001). After the 7 th ECT, SOD values were significantly lower than pre-ECT SOD values (p<0.05, Z= -3,459). There were no significant difference between pre-and post-ECT values of MDA, NO, and XO (p>0.05). However, pre-ECT SOD values were significantly and positively correlated with pre-ECT HDRS scores (r=0.641, p=0.007). Conclusion:The decrease in antioxidant enzyme SOD after ECT may damage the neurons by increasing oxidative stress. Thus, possible benefits of antioxidant supplementation during ECT should be investigated. Additionally, higher pre-ECT o...

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Chronic electroconvulsive shock and neurotransmitter receptors - An update -

Cited by 58 publications

References 124 publications

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Repeated electroconvulsive shock produces long-lasting increases in messenger RNA expression of corticotropin-releasing hormone and tyrosine hydroxylase in rat brain. Therapeutic implications.

Catecholamine overflow within rat striatum: the influence of microstimulation and electroconvulsive stimulation as observed with voltammetry

Depresyonda EKT Sonrası Süperoksit Dismutaz Aktivitesi Düşüyor ve EKT'ye Kötü Yanıtla Korelasyon Gösteriyor

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