OBJECTIVE: The interaction between MK-801, a model of psychosis and KCl-induced depolarization or electroconvulsive shock (ECS), a therapeutic model of electroconvulsive therapy (ECT), was investigated in SH-SY5Y cells and the rat frontal cortex. METHODS: SH-SY5Y cells were pretreated with 1 microM MK-801 for 15 min, followed by cotreatment with 100 mM KCl for 5 min. MK-801 was reintroduced after the KCl was washed out, and the samples were incubated before harvesting. For the experiments in rats, male Sprague-Dawley rats were treated with MK-801 followed by ECS. Immunoblot analyses of glycogen synthase kinase 3beta (GSK3beta) (Ser9), AKT (Ser473) and extracellular legulated kinase (ERK)1/2 in SH-SY5Y cells and the rat frontal cortex were performed. RESULTS: KCl-induced neuronal depolarization resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), followed by increased phosphorylation of the enzymes in SH-SY5Y cells. Cotreatment with MK-801 and KCl inhibited the initial dephosphorylation of AKT and GSK3beta produced by KCl-induced neuronal depolarization. Similarly, ECS resulted in the transient dephosphorylation of AKT (Ser473) and GSK3beta (Ser9), whereas cotreatment with MK-801 inhibited the initial dephosphorylation of AKT (Ser473) and GSK3beta (Ser9) produced by ECS in the rat frontal cortex. No significant interaction was observed between MK-801 and KCl in the dephosphorylation of ERK1/2. CONCLUSION: These results suggest that an antagonistic interplay between MK-801 and neuronal depolarization by KCl or ECS is involved the regulation of AKT (Ser473) and GSK3beta (Ser9) phosphorylation.
Animals ; Dizocilpine Maleate* ; Electroconvulsive Therapy ; Electroshock ; Glycogen Synthase Kinases ; Humans ; Male ; Neurons* ; Phosphorylation ; Phosphotransferases ; Psychotic Disorders ; Rats* ; Rats, Sprague-Dawley

BACKGROUND: Electroconvulsive(ECT) or electroshock therapy(EST) remains controversial and its indications are still the subject of discussion. Despite both medical and legal opposition, it is still widely practiced. The aim of ECT is to produce a grand mal seizure rather than the electrical stimulus which is responsible for the therapeutic effect. This causes widespread physiological changes, particularly affecting the cardiovascular and nervous system. The anesthetic agents for ECT should provide a smoooth rapid induction, a rapid recovery and attenuation of the physiologic effect of ECT. METHODS: Propofol(1 mg/kg) and thiopental sodium(2 mg/kg) were compared as anesthetic agents for ECT in 20 patients on four occasions in a repeated measure crossover study. In each patients receiving propofol or thiopental sodium on different occasions, arterial pressure, heart rate, seizure duration and recovery time were recorded. RESULTS: The incidence of discomfort on injection was significantly higher with propofol (47.5%) compared to thiopental sodium (2.5%). The duration of seizure with propofol was 37+/-11.3 sec and thiopental sodium was 41.2+/-11.6 sec but it was not significant(P=0.11). The increase in systolic and diastolic arterial pressure and heart rate were higher with thiopental sodium. Recovery time was significantly shorter with thiopental sodium (476.5+/-47.7 sec) compares to propofol (506.6+/-62.2 sec) (P<0.05). CONCLUSIONS: Propofol is more effective than thiopental sodium at obtunding the hypertensive to ECT without causing significant hypotention.
Anesthetics ; Arterial Pressure ; Cross-Over Studies ; Electroconvulsive Therapy* ; Electroshock ; Heart Rate ; Humans ; Incidence ; Nervous System ; Propofol* ; Seizures ; Thiopental*

Electroconvulsive shock (ECS) induces not only an antidepressant effect but also adverse effects such as amnesia. One potential mechanism underlying both the antidepressant and amnesia effect of ECS may involve the regulation of serotonin (5-hydroxytryptamine) 6 (5-HT6) receptor, but less is known about the effects of acute ECS on the changes in 5-HT6 receptor expression in the hippocampus. In addition, as regulation of 5-HT receptor expression is influenced by the number of ECS treatment and by interval between ECS treatment and sacrifice, it is probable that magnitude and time-dependent changes in 5-HT6 receptor expression could be influenced by repeated ECS exposure. To explore this possibility, we observed and compared the changes of 5-HT6 receptor immunoreactivity (5-HT6 IR) in rat hippocampus at 1, 8, 24, or 72 h after the treatment with either a single ECS (acute ECS) or daily ECS for 10 days (chronic ECS). We found that acute ECS increased 5-HT6 IR in the CA1, CA3, and granule cell layer of hippocampus, reaching peak levels at 8 h and returning to basal levels 72 h later. The magnitude and time-dependent changes in 5-HT6 IR observed after acute ECS were not affected by chronic ECS. These results demonstrate that both acute and chronic ECS transiently increase the 5-HT6 IR in rat hippocampus, and suggest that the magnitude and time-dependent changes in 5-HT6 IR in the hippocampus appear not to be influenced by repeated ECS treatment.
Amnesia ; Animals ; Electroshock* ; Hippocampus* ; Rats* ; Serotonin

No abstract available.
Animals ; Biogenic Amines* ; Brain* ; Electroshock* ; Rats*

No abstract available.
Animals ; Brain Stem* ; Brain* ; Electroshock* ; Hypothalamus* ; Mice*

No abstract available.
Amnesia, Anterograde* ; Animals ; Cholinergic Agents* ; Electroshock* ; Rats*

OBJECTIVES: Both electroconvulsive shock(ECS) and kainic acid-induced seizures activate mitogenactivated protein kinases(MAPKs)in rat hippocampus. They can also induce the expression of MAPK phosphatase-1(MKP-1)in rat hippocampus. MKP-1 is known as a specific MAPK deactivator. This study aimed to elucidate the role of MKP-1 in the deactivation of MAPKs in rat hippocampus. METHODS: In order to induce MKP-1 in the hippocampus, ECS was given to the rats. At the time points when MKP-1 was sufficiently induced, the second ECS was given to them and the subsequent phosphorylation or activation of MAPKs were measured in the hippocampus. A second group of rats were injected with kainic acid and the relationship between MKP-1 expression and MAPK phosphorylation was examined in their hippocampi. RESULTS: The expression of MKP-1 did not influence the phosphorylation or activation of MAPKs following ECS in rat hippocampus. Kainic acid-induced expression of MKP-1 did not significantly reduce the phosphorylation of MAPKs. CONCLUSION: MKP-1 did not play a significant role in the deactivation of MAPKs which were activated by ECS or kainic acid in rat hippocampus.
Animals ; Electroshock ; Hippocampus* ; Kainic Acid ; Phosphorylation ; Rats* ; Seizures

OBJECTIVES: The N-methyl-D-aspartate (NMDA) receptor plays an important role in synaptic plasticity. The functional NMDA receptor is an oligomer of several subunits and the most abundant subunits in the brain are NR1, NR2A and NR2B. The function of the NMDA receptor is regulated by protein phosphorylation and by changes in the level of protein expression. The present study examined the effect of repeated electroconvulsive shock (ECS), an effective antidepressant and antipsychotic measure, on the expression of NMDA receptor subunit proteins in the rat hippocampus. METHODS: Male Sprague-Dawley rats were given 1, 5, or 10 consecutive daily ECS and the amounts of NR1, NR2A, and NR2B in the hippocampus were assessed by the immunoblot analysis. RESULTS: The expression levels of NR1 and NR2A subunits were found positively correlated with the number of treatment. However, there was no evidence of NR2B regulation by ECS. CONCLUSION: These findings suggest the action of ECS in the regulation of the NMDA receptor, and hence in the regulation of synaptic plasticity.
Animals ; Brain ; Electroshock* ; Hippocampus* ; Humans ; Male ; N-Methylaspartate* ; Phosphorylation ; Plastics ; Rats* ; Rats, Sprague-Dawley

No abstract available.
Animals ; Electroshock* ; Glutamate Decarboxylase* ; Glutamate-Ammonia Ligase* ; Glutamic Acid* ; Glutamine* ; Hippocampus* ; Rats*

OBJECTIVES: ECS could have therapeutic effects on psychiatric illnesses by inducing IEGs, which in turn regulates expression of their target genes. We observed AP-1 binding activity and identified AP-1 binding proteins in NMDAR1, late response gene of IEGs, which considered as the candidate gene for schizophrenia. METHODS: By gel shift assay and supershift assay, we observed binding activities and AP-1 binding proteins in NMDAR1. Because IEGs are induced rapidly but transiently by external stimuli, there is a possibility that the expression of IEGs is negatively feedbacked by their own products via their AP-1 binding sites. For that purpose, we also observed AP-1 binding activity of c-fos and c-jun via gel shift and supershift assay. RESULTS: ECS increased AP-1 binding activities of NMDAR1 gene, contributed by c-Fos and its related proteins. Peak of the increased binding was 60 minutes in both hippocampus and cerebellum. Though expression of c-Fos and c-Jun were increased by ECS, there were no changes in AP-1 binding activities after ECS. AP-1 sites of IEGs were binded by CREB, regardless of ECS. CONCLUSION: There is a possibility that ECS induced IEG expression, and then incresed expression of NMDR1 by binding of expressed IEGs to the AP-1 site of NMDAR1. ECS did not increase AP-1 binding activities of IEGs. This suggests that the regulation of IEGs' expression can not be influenced mainly by AP-1 site.
Animals ; Binding Sites ; Brain* ; Carrier Proteins ; Cerebellum ; Electroshock* ; Hippocampus ; Rats* ; Schizophrenia ; Transcription Factor AP-1*