• Korean Journal of Biological Psychiatry
• /
• v.3 no.2
• /
• pp.181-190
• /
• 1996

To clarify the mechanism of action of electroconvulsive shack(ECS) in respect to molecular biology, and to detect the quantitative amount of change of c-fos gene expression after ECS in the rat's brain, the authors obtained brain specimens from the striatum, cerebral cortex, hippocampus, and cerebellum. Each brain was removed within 30min. after ECS(130V, 0.5sec) and ECS-sham. Then we performed RT-PCR. The results are 1) ECS was found to affect the expression of immediate early genes. 2) the cerebral cortex and hippocampus was more influenced by ECS thon in the cerebellum and striatum. From these results, we can suggest that ECS is related to the mechanism of cognition, mood, memory which is correlated to cerebral cortex and hippocampus.

• Sleep Medicine and Psychophysiology
• /
• v.1 no.1
• /
• pp.87-98
• /
• 1994

Objectives: To examine a defect in inhibitory gating of auditory evoked response in schizophrenics, to compare P3 latency and amplitude in negative and positive schizophrenics, and to assess the association of P3 with family history of the psychiatric disorders, electroconvulsive therapy, and clinical features. Methods: 54 schizophrenics(male 31, female 23) and 75 controls(male 33, female 42) were tested with event-related potential paradigm designed to elicit P3 response and Frankfurter Beschwerde Fragebogen. Results: In schizophrenics, the latency of P3 was significantly more delayed and the amplitude of P3 was significantly more reduced than in the controls. Significant differences in P3 latency and amplitude between negative and positive schizophrenics were not found. And significant difference in the P3 latency and amplitude between schizophrenics with family histories of psychiatric disorder and those without family histories of psychiatric disorder was not found also. The P3 latency and amplitude was not significantly related with electroconvulsive therapy and other clinical features such as age, duration of illness, onset of inllness, number of admission, and doses of antipsychotics etc. Conclusion: These results suggested that schizophrenics had a dysfunction in the process of selective attention and that P3 was not significantly related with family history of the psychiatric disorders, positive and negative symptoms, electro1convulsive therapy, and clinical features in schizophrenics.

• The Korean Journal of Pharmacology
• /
• v.27 no.1
• /
• pp.13-20
• /
• 1991

There are some rather conflicting reports correlating ECS-induced changes of brain acetylcholine, and recently, Zawia and Bondy(1990) proposed the biological role of polyamine system in the long-term adaptive responses of brain to electrical stimulation. This study was undertaken to evaluate the effects of a single or repeated ECS(10mA, 100cps, 1sec; 5 ECS spread out over 9 days) on the brain acetylcholine(ACh) and polyamine contents of male mice. The ACh contents of temporal cortex(TCx) and decorticated cerebrum(dc-CB) were markedly increased by 79.9% and 49.4%, respectively, 10 and 30 min after ECS, and the increases were significantly attenuated with repeated 5 ECS, particularly in dc-CB. The putrescine concentrations of both TCx and dc-CB were little different and not affected by 1 ECS or 5 ECS. But the spermidine(Sd) concentration was higher in dc-CB and spermine(Sm) higher in TCx. While they were moderately decreased after 1 ECS, and their decreases were accentuated after 5 ECS, particularly in dc-CB.Sm(30mg/kg, i.p. inject. 30min before ECS) did not affect the ECS-induced increase of ACh content. Thease results suggest that both of brain ACh and polyamine may be implicated with the long-term adaptive responses to electrical stimulation

• The Korean Journal of Pharmacology
• /
• v.28 no.2
• /
• pp.115-128
• /
• 1992

The training of male wistar rats for active conditioned response (ACR) was performed by one daily training session of 30 consecutive trials for 10 successive days using a two-way shuttle box, and the rats that showed 10 or more ACRs on the last day were treated for further 10 days with electroconvulsive shock (ECS : 50 mA, 0.5 msec; 100 Hz; 1.5 sec) and the following compounds. On the 20th day, all the rats were tested for the ACR rention. The ECS regimens were one ECS per day for 10 days with one day interval $(5{\times}ECS)$, one ECS at 3 hrs (ECS-3h), and one ECS at 24 hrs (ECS-24h), respectively, before the ACR retention test. And CDP-choline (cc: 250 mg/kg), spermine (SM: 10 mg/kg), ${\alpha}-difluoromethylornithine$ (DO: 250 mg/kg), or aminoguanidine (AG: 100 mg/kg) was administered by one daily i.p. injection for 10 days. The ACR number $(13.7{\pm}1.0)$ obtained on the last training day was increased by 37.23% on the 20th day in the control rats. And the ACR increase was significantly suppressed by 5-ECS, ECS-3h, CC, or SM but was little affected by ECS-24h, DO, or AG. However, the 5-ECS induced impairment of ACR retention was significantly suppressed by AG, SM, and CC in the order of potency but was little affected by DFMO. And the ECS-3h induced impairment was moderately worsened by SM or AG. The acetylcholine (ACh) of the rat hypothalamus (HT), hippocampus (HC), and entorhinal cortex (EC) was markedly increased by CC and moderately increased by SM, but little affected by ECS-3h, ECS-24h, DO, or AG. But $5{\times}ECS$ slightly increased the ACh content. The brain putrescine (Pt) content was significantly increased by AG and little affected by CC, SM, or DO. But the $5{\times}ECS$ markedy decreased the brain Pt content, and the decrease was significantly suppressed by CC, SM, or AG. CC induced the marked increases of the spermidine (Sd) and spermine (Sm) contents of all the areas. SM increased the Sd contents of all the areas and the EC-Sm content. DO decreased the brain Sd and Sm contents. And AG increased the HT-Sd content and the Sm contents of all the brain areas. The $5{\times}ECS$ induced decrease of the HC-Sm content was suppressed by CC, SM and AG. These results suggest that the improving effect of aminoguanidine on the $5{\times}ECS$ induced impairment of ACR retention may be ascribed in part to its activity as a diamine oxidase inhibitor.