• 사상체질의학회지
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• 제11권2호
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• pp.283-299
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• 1999

1. 연구목적 kainic acid를 실험동물에 주입할 경우 간질발작을 일으키고 변연계 특히 해마체 부위에서 조직의 손상이 일어나게 되는데 이는 사람에 있어 측두엽성 간질에서 보이는 구조적 변화와 유사한 것이다. 본 실험은 신경독성 물질인 kainic acid로 마우스의 해마체에 손상을 유발하고 이 경우에 열다한소탕이 신경보호효과가 있는지의 여부를 알고자한 것이다. 2. 연구방법 kainic acid를 경구투여하고 열다한소탕을 3주일간 복용시키면서 각각 1, 2, 3일과 1주, 3주에 조직을 관찰하였다. 조직손상은 해마체의 CA1, CA3과 thalamus, amygdala 등에서 c-fos 와 DNA fragmentation의 출현 율로 지표를 삼았으며 광학현미경하에서 육안적 관찰을 병행하였다. 3. 결과 및 결론 kainic acid만을 투여한 대조 군에서는 실험 3주째에도 손상지표인 c-fos 와 DNA fragmentation이 발견되었으나 열다한소탕을 투여한 실험 군에서는 실험 약 3일 째부터 손상지표의 발현이 줄어 7일째에는 나타나지 않음을 알 수 있었다. 또한 현미경 하의 육안적 관찰에서도 실험초기 많은 손상을 보였던 신경세포가 2주일 후 어느 정도 회복되는 것을 볼 수 있었다. 이로써 열다한소탕이 kainic acid로 유발된 실험동물의 해마체손상에 대하여 신경세포 보호 효과 및 손상 억제 효과가 있음을 알 수 있었다.

• Applied Microscopy
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• 제22권1호
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• pp.79-88
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• 1992

In order to identify the effects of the kainic acid in the retina kainic acid (120 nmol/$5{\mu}l$) were injected through the pars plana of the ciliary body into the duck eye ball at 7th day after hatching. The animals were sacrificed by decapitation on the 1st, 4th and 10th day after injection of the kainic acid. The specimen was processed for the light and electron microscopes respectively. The results obtained were as followings 1. The inner nuclear, inner plexiform and ganglion cell layers of the retina showed marked changes in all of the groups. 2. The cells in the inner nuclear layer showed marked degenerative changes of the organelles including the pyknoses and destruction of the nucleus on the 1st day after injection. These destructive changes of the cells were progressively disappeared until the 10th day after injection. 3. After injection of the kainic acid the neurites of the inner plexiform layer were swollen at the first, and thereafter those changes were gradually disappeared until the 10th day. 4. In the ganglion cell defected by the kinic acid, the enlargement and segmentation of the endoplasmic reticulum and pyknosis of the nucleus were-observed in all the groups, although the lipid droplets were only shown in the 4th day. From the above results, the evidence suggests that kainic acid gives to the toxic effect on the nuurons of the retina with exception of the photoreceptors.

• 대한수의학회지
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• 제26권2호
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• pp.221-224
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• 1986

Kainic acid가 오리 망막에 미치는 영향을 알아보기 위하여 kainic acid $50{\mu}l$($1.0{\mu}mol$)를 오리의 안구내로 주입한 후 망막을 경시적으로 관찰하였던 바 다음과 같은 결과를 얻었다. 주사후 8시간째 망막의 내내핵층과 내망상층에서 공포화가 인정되었고 24시간째는 내핵층에서 핵농축이 현저하였으며 48시간째의 예에서는 농축된 핵이 상당수 소실되면서 망막의 두께도 다소 얇게 나타났다. 주사후 96시간과 10일째는 내핵층을 구성하는 대부분의 세포가 소실되어 망막의 두께가 상당히 얇아졌고 내망상층의 두께도 경시적으로 얇아지는 경향이었다.

• 약학회지
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• 제7권1호
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• pp.8-12
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• 1963

The piperazine salts with 24 kinds of phenols and 6 kinds of organic carboxylic acids were prepared. The test of anthelmintic effect against Ascaris suilla, in vitro, for Hexachlorophene-piperazine salt, Bithionol-piperazine salt, Kainic acid-piperazine salt were also carried out compared with piperazine, Hexachlorophene, Bithionol and Kainic acid.

• The Korean Journal of Physiology and Pharmacology
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• 제11권4호
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• pp.149-154
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• 2007

Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element modulatory factor 1, neurexin III, ND4, ATPase, $H^+$ transporting, V1 subunit E isoform 1, and N-myc downstream regulated gene 2. Although the functions of these genes and their products remain to be determined, their identification provides insight into the molecular mechanism(s) involved in KA-induced neuronal cell death in the hippocampal CA3 area.

• 대한한의학회지
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• 제31권5호
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• pp.167-178
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• 2010

Objectives: The present study investigated the effects of acupuncture treatment and their mechanism by using the kainic acid (KA)-induced epilepsy mouse model. Materials and Methods: The seizure was induced by an intraperitoneal (i.p.) injection of 30 mg/kg KA, and the acupuncture treatment was subsequently administered to acupoint Shaofu(HT8) bilaterally with two pretreatment sessions before injection (total 3 times over 3 days). Twenty four hours after injection, we observed the survival of neuronal cells in the CA3 region of the hippocampus. In addition, the activation of microglia and astrocytes was observed by using CD11b and GFAP immunohistochemistry in the same region. Results: The results indicate that acupuncture treatment reduced the rate of neural cell death in the CA3 region of the hippocampus and decreased the activations of microglia and astrocytes in this region. Conclusion: These results demonstrate that acupuncture treatment protects hippocampal neuronal cell death from KA-induced epileptic seizure by inhibiting the activations of microglia and astrocytes.

• Journal of Yeungnam Medical Science
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• 제35권2호
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• pp.192-198
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• 2018

Background: Chronic inflammation can lower the seizure threshold and have influence on epileptogenesis. The components of red ginseng (RG) have anti-inflammatory effects. The abundance of peripherally derived immune cells in resected epileptic tissue suggests that the immune system is a potential target for anti-epileptogenic therapies. The present study used continuous electroencephalography (EEG) to evaluate the therapeutic efficacy of RG in intrahippocampal kainic acid (IHKA) animal model of temporal lobe epilepsy. Methods: Prolonged status epilepticus (SE) was induced in 7-week-old C57BL/6J mice via stereotaxic injection of kainic acid (KA, 150 nL; 1 mg/mL) into the right CA3/dorsal hippocampus. The animals were implanted electrodes and monitored for spontaneous seizures. Following the IHKA injections, one group received treatments of RG (250 mg/kg/day) for 4 weeks (RG group, n=7) while another group received valproic acid (VPA, 30 mg/kg/day) (VPA group, n=7). Laboratory findings and pathological results were assessed at D29 and continuous (24 h/week) EEG monitoring was used to evaluate high-voltage sharp waves on D7, D14, D21, and D28. Results: At D29, there were no differences between the groups in liver function test but RG group had higher blood urea nitrogen levels. Immunohistochemistry analyses revealed that RG reduced the infiltration of immune cells into the brain and EEG analyses showed that it had anticonvulsant effects. Conclusion: Repeated treatments with RG after IHKA-induced SE decreased immune cell infiltration into the brain and resulted in a marked decrease in electrographic seizures. RG had anticonvulsant effects that were similar to those of VPA without serious side effects.

• 동의생리병리학회지
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• 제28권6호
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• pp.614-620
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• 2014

Kainic acid (KA) is a excitatory agonist causing epileptic seizure and excitotoxicity in the hippocampus. Gastrodia Elata (GE) is known to have anti-convulsant and anti-oxidant effects. This study was investigated a possible role of GE in suppressing epileptic seizure using KA-induced epilepsy mouse model. Eight-week-old male C57BL/6 mice were administrated GE (50 or 500 mg/kg) once a day for 5 days, and then injected KA (30 mg/kg) intraperitoneally. Behavioral changes in mice by KA were evaluated for 90 minutes immediately after the KA administration. Six hours after the KA administration, their brains were harvested and the expressions of glutamate decarboxylase 67 (GAD-67) and K+-Cl- cotransporter 2 (KCC2) in the hippocampus of the mice were measured by immunohistochemistry.GE delayed the onset of epileptic seizure after KA administration, suppressed the severity of the seizure and decreased the number of severe seizures dose dependently. Moreover, GAD-67 and KCC2 expressions in the cornu ammonis (CA) 1 and CA3 of 500 mg/kg GE administrated mice were significantly increased compared to those in KA-treated mice.GAD-67 and KCC2 play an important role in regulating GABAergic system. Our results suggest that GE has anti-convulsant effect against KA-induced epileptic seizure through enhancing GABAergic system.

• Biomolecules & Therapeutics
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• 제4권2호
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• pp.167-173
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• 1996

This study was undertaken to evaluate a behavior-electroencephalogram (EEG) pattern relationship in pilocarpine- and kainic acid-induced convulsions of rats. Also we intended to examine the effect of a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801, and diazepam on the pilocarpine-induced behavioral and electrical seizures in rats. The electrical activities at frontal and hippocampal areas and behavior activities were measured in freely moving rats. At the beginning of the experiments, the rats displayed an exploratory behavior. This awake and moving phase with a low amplitude, irregular, 4-10 Hz wave was followed by a still phase. Pilocarpine (400 mg/kg, i.p.) and kainic acid (0.5 mg/kg, i.c.v.) induced tonic and clonic seizures. The pilocarpine-induced change in electrical activities exhibited a weak correlation with behavioral convulsion at all stages. The amplitude and duration of the electrical response were not linear with the degree of behavioral score. An application of MK-801 (dizocilpine, 7.5 mg/kg) did not affect the amplitudes of the convulsant-induced electrical activities, though the same dose of this drug caused the deformation of the electrical pattern. There was no effect of MK-801 on the behavioral and electrical activities as expected. Diazepam (1 mg/kg) did not affect the amplitude of the electrical activities induced by pilocarpine but changed the pattern of these activities. Our study shows that there is no linear relationship between degree of behavior and amplitude of electrical activities of convulsants. This may indicate that the NMDA receptor stimulation can be processed by the neocortical or hippocampal network in a different way between behavioral and electrical activities.

• 한국감성과학회:학술대회논문집
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• 한국감성과학회 2009년도 추계학술대회
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• pp.190-192
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• 2009

Kainic acid (KA), an agonist for kainate and AMPA receptors, is an excitatory neurotoxic substance. Vitamin E such as alpha-tocopherol and alpha-tocotrienol is a chain-breaking antioxidant, preventing the chain propagation step during lipid peroxidation. In the present study, we have investigated the neuroprotective effects of alphatocopherol and alpha-tocotrienol on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC). After 15h KA treatment, delayed neuronal death was detected in CA3 region. Alpha-tocopherol and alpha-tocotrienol increased cell survival and reduced the number of TUNEL-positive cells in CA3 region. These data suggest that alpha-tocopherol and alpha-tocotrienol treatment have protective effects on KA-induced cell death