Acute and chronic electroconvulsive shock in rats: Effects on peripheral markers of neuronal injury and glial activity

Busnello, João Vicente; Leke, Renata; Oses, Jean Pierre; Feier, Gustavo; Bruch, Ricardo; Quevedo, João; Kapczinski, Flávio; Souza, Diogo O.; Portela, Luis Valmor

doi:10.1016/j.lfs.2005.11.028

Cited by 36 publications

(18 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These findings suggest that repeated ECS inactivates the apoptotic machinery to exert its protective activities, and c-Myc and Bad may play an important role in the therapeutic action of ECT, in agreement with previous reports demonstrating that ECS elicits trophic action in the brain (Kondratyev et al, 2001;Hellsten et al, 2002;Kim et al, 2005;Madsen et al, 2005;Busnello et al, 2006;Wennstrom et al, 2006). In conclusion, the present findings further support the neuroprotective effect of ECS, and facilitate our understanding of the mechanism of action of ECT as a neurotrophic stimulus.…”

Section: Discussionsupporting

confidence: 92%

“…The therapeutic effect of ECT requires multiple administrations, and repeated electroconvulsive seizure (ECS), an animal model for ECT, exerts trophic activity, including neuroprotective and proliferative effects, in the brain. ECS may prevent neuronal apoptosis induced by kainic acid (Kondratyev et al, 2001), decrease neuronal death (Busnello et al, 2006), and counteract corticosteroneinduced inhibition of neurogenesis and gliogenesis (Hellsten et al, 2002;Wennstrom et al, 2006). The majority of reports have focused on the hippocampus regarding the trophic effects of ECS (Hellsten et al, 2002;Wennstrom et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Repeated electroconvulsive seizure induces c-Myc down-regulation and Bad inactivation in the rat frontal cortex

et al. 2008

View full text Add to dashboard Cite

Repeated electroconvulsive seizure (ECS), a model for electroconvulsive therapy (ECT), exerts neuroprotective and proliferative effects in the brain. This trophic action of ECS requires inhibition of apoptotic activity, in addition to activation of survival signals. c-Myc plays an important role in apoptosis of neurons, in cooperation with the Bcl-2 family proteins, and its activity and stability are regulated by phosphorylation and ubiquitination. We examined c-Myc and related proteins responsible for apoptosis after repeated ECS. In the rat frontal cortex, repeated ECS for 10 days reduced the total amount of c-Myc, while increasing phosphorylation of c-Myc at Thr58, which reportedly induces degradation of c-Myc. As expected, ubiquitination of both phosphorylated and total c-Myc increased after 10 days ECS, suggesting that ECS may reduce c-Myc protein level via ubiquitination-proteasomal degradation. Bcl-2 family proteins, caspase, and poly(ADP-ribose) polymerase (PARP) were investigated to determine the consequence of down-regulating c-Myc. Protein levels of Bcl-2, Bcl-XL, Bax, and Bad showed no change, and cleavage of caspase-3 and PARP were not induced. However, phosphorylation of Bad at Ser-155 and binding of Bad to 14-3-3 increased without binding to Bcl-X L after repeated ECS, implying that repeated ECS sequesters apoptotic Bad and frees pro-survival Bcl-XL. Taken together, c-Myc down-regulation via ubiquitination-proteasomal degradation and Bad inactivation by binding to 14-3-3 may be anti-apoptotic mechanisms elicited by repeated ECS in the rat frontal cortex. This finding further supports the trophic effect of ECS blocking apoptosis as a possible therapeutic effect of ECT.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Repeated electroconvulsive seizure induces c-Myc down-regulation and Bad inactivation in the rat frontal cortex

et al. 2008

View full text Add to dashboard Cite

show abstract

“…It was demonstrated to be an important independent predictor of psychosocial morbidity in subjects with severe obesity [1]. 12-to 30-fold higher than in the general population, and one important characteristic of the morbid obesity condition is the presence of central obesity, which means large belly and neck circumferences [2]. Especially related to having a thick neck is the high incidence of OSAHS [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

“…NSE is a glycolytic pathway enzyme, which the γγ isoform is predominantly found in neuronal tissue. As NSE is not physiologically secreted, increases in its peripheral levels have been specifically related to neuronal injury, as reported in traumatic brain, injury stroke, and epileptic seizures [11,12].…”

Section: Introductionmentioning

confidence: 99%

Serum S100B but not NSE Levels are Increased in Morbidly Obese Individuals Affected by Obstructive Sleep Apnea–Hypopnea Syndrome

et al. 2008

View full text Add to dashboard Cite

show abstract

“…The extracellular activity of S100B is concentration-dependent; in nanomolar concentration, S100B enhances neurite growth and survival of brain cells; while in micromolar concentration, S100B is toxic to neuronal cells and considered a biomarker of brain damage and neurodegeneration [23] . In a rat model of ECS, Busnello et al [24] reported that there is an alteration of the S100b protein level in CSF of rats under chronic ECS, indicating a protective activity of astrocytes in the brain under chronic ECS. In this study, we found increased expression of S100b mRNA in the frontal cortices of rats under repeated ECS, which may contribute to the therapeutic efficacy of ECT.…”

Section: Discussionmentioning

confidence: 99%

Identification of Gene Transcripts in Rat Frontal Cortex That Are Regulated by Repeated Electroconvulsive Seizure Treatment

Huang

Chen²

2008

Neuropsychobiology

View full text Add to dashboard Cite

Background/Aims: Electroconvulsive therapy (ECT) is an effective treatment modality for severe psychiatric disorders. Many studies have suggested that the therapeutic efficacy of ECT can be attributed to the structural and functional readjustment of the brain cells, which is mediated by differential gene expression in the brain. The aim of this study is to understand the molecular mechanism of ECT. Methods: We used microarray-based gene expression profiling technology and real-time quantitative PCR (RT-qPCR) to screen differentially expressed genes in the brain in a rat model of ECT. Results: Four upregulated and three downregulated genes were identified in this study. The 4 upregulated genes are S100 protein, beta polypeptide (S100b), S100 calcium binding protein A13_predicted (S100a13_predicted), diazepam-binding inhibitor (Dbi), and YKT6 homolog (S. Cerevisiae) (Ykt6), respectively; while the 3 downregulated genes are basigin (Bsg), histidine triad nucleotide binding protein 1(Hint 1), and neural precursor cell expressed, developmentally downregulated gene 8 (Nedd8), respectively. Conclusion: In view of the neurobiological function of these genes and their relevance to mental disorders, repeated ECS can affect gene expression involved in the neurotransmission and synaptic plasticity, which may account for the clinical effects of ECT.

show abstract

Acute and chronic electroconvulsive shock in rats: Effects on peripheral markers of neuronal injury and glial activity

Cited by 36 publications

References 37 publications

Repeated electroconvulsive seizure induces c-Myc down-regulation and Bad inactivation in the rat frontal cortex

Repeated electroconvulsive seizure induces c-Myc down-regulation and Bad inactivation in the rat frontal cortex

Serum S100B but not NSE Levels are Increased in Morbidly Obese Individuals Affected by Obstructive Sleep Apnea–Hypopnea Syndrome

Identification of Gene Transcripts in Rat Frontal Cortex That Are Regulated by Repeated Electroconvulsive Seizure Treatment

Contact Info

Product

Resources

About