• 한국감성과학회:학술대회논문집
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• 한국감성과학회 2008년도 추계학술대회
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• pp.147-150
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• 2008

Vitamin C ascorbic acid (AA) and dehydroascorbic acid (DHA) as an antioxidant have been shown to have protective effects in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effect of AA and DHA on Kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures (OHSC). After 12h KA treatment, significant delayed neuronal death was detected in CA3 region, but not in CA1. Intermediate dose of AA and DHA pretreatment significantly prevented cell death and inhibit ROS level, mitochondrial dysfunction and capase-3 activation in CA3 region. In the case of low or high dose, however, AA or DHA pretreatment were not effective. These data suggest that both AA and DHA pretreatment have neuroprotective effects on KA-induced neuronal injury depending on the concentration, by means of inhibition of ROS generation, mitochondrial dysfunction, and caspase-dependent apoptotic pathway.

• Molecules and Cells
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• 제25권1호
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• pp.124-130
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• 2008

Astrocyte ion channels participate in ionic homeostasis in the brain. Inward rectifying potassium channels (Kir channels) in astrocytes have been particularly implicated in $K^+$ homeostasis because of their high open probability at resting potential and their increased conductance at high concentrations of extracellular $K^+$. We examined the expression of the Kir2.1 subunit, one of the Kir channel subunits, in the mouse brain by immunohistochemistry. Kir2.1 channels were widely distributed throughout the brain, with high expression in the olfactory bulb and the cerebellum. Interestingly, they were abundantly expressed in astrocytes of the olfactory bulb, while astrocytes in other brain regions including the hippocampus did not show any detectable expression. However, Kir2.1 channel-expressing cells were dramatically increased in the hippocampus by kainic acid-induced seizure and the cells were glial fibrillary acidic protein (GFAP)-positive, which confirms that astrocytes in the hippocampus express Kir2.1 channels under pathological conditions. Our results imply that Kir2.1 channels in astrocyte may be involved in buffering $K^+$ against accumulated extracellular $K^+$ caused by neuronal hyperexcitability under phathophysiological conditions.

• 대한약침학회지
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• 제19권2호
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• pp.163-166
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• 2016

Objectives: Quercetin is a flavonoid and an important dietary constituent of fruits and vegetables. In recent years, several pharmacological activities of quercetin, such as its neuroprotective activity and, more specifically, its anti-convulsant effects in animal models of epilepsy, have been reported. This study evaluated the role of quercetin pretreatment on gene expression of ${\gamma}$-amino butyric acid type A ($GABA_A$) receptor beta subunits in kainic acid (KA)-induced seizures in mice. Methods: The animals were divided into four groups: one saline group, one group in which seizures were induced by using KA (10 mg/kg) without quercetin pretreatment and two groups pretreated with quercetin (50 and 100 mg/kg) prior to seizures being induced by using KA. Next, the messenger ribonucleic acid (mRNA) levels of the $GABA_A$ receptor ${\beta}$ subunits in the hippocampus of each animal were assessed at 2 hours and 7 days after KA administration. Quantitative real-time polymerase chain reaction (RT-PCR) assay was used to detect mRNA content in hippocampal tissues. Results: Pretreatments with quercetin at doses of 50 and 100 mg/kg prevented significant increases in the mRNA levels of the ${\beta}_1$ and the ${\beta}_3$ subunits of the $GABA_A$ receptor at 2 hours after KA injection. Pretreatment with quercetin (100 mg/kg) significantly inhibited ${\beta}_1$ and ${\beta}_3$ gene expression in the hippocampus at 7 days after KA injection. But, this inhibitory effect of quercetin at 50 mg/kg on the mRNA levels of the ${\beta}_3$ subunit of the $GABA_A$ receptor was not observed at 7 days after KA administration. Conclusion: These results suggest that quercetin (100 mg/kg) modulates the expression of the $GABA_A$ receptor ${\beta}_1$ and ${\beta}_3$ subunits in the KA model of epilepsy, most likely to prevent compensatory responses. This may be related to the narrow therapeutic dose range for the anticonvulsant activities of quercetin.

• Journal of Ginseng Research
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• 제33권1호
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• pp.48-54
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• 2009

Epileptifrom discharges were induced in the telencephalon of the adult zebrafish via perfusion with pentylenetetrazole (PTZ), bicuculline methiodide, kainic acid-treated artificial cerebrospinal fluid (aCSF), and $Mg^{2+}$-free aCSF. Ginseng total saponin [GTS ($50{\mu}g/ml$)] was shown to attenuate the occurrence rate of epilpetiform discharges by 50-75%, compared to the control. Ginsenoside $Rg_1$ ($130{\mu}M$) reduced the epileptiform discharges in the isolated telencephalon and delayed the occurrence of behavioral seizures observed from the adult zebrafish placed in the PTZ (10 mM)-containing aquarium water. However, Re was not effective in the suppression of epileptiform discharges and behavioral seizures. These results indicate that $Rg_1$ may be useful in the control of epileptiform discharges and effective in controlling behavioral seizures, and that the zebrafish can be used as a model animal for the testing of potential anticonvulsant drugs.

• The Korean Journal of Physiology and Pharmacology
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• 제7권6호
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• pp.307-310
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• 2003

Kainic acid (KA) is a structural analogue of glutamate that interacts with specific presynaptic and postsynaptic receptors to potentiate the release and excitatory actions of glutamate. Systemic or intracerebroventricular (i.c.v.) administration of KA to experimental animals elicits multifocal seizures with a predominantly limbic localization, and results in neuronal death of cornu ammonia 1 (CA1), reactive gliosis and biochemical changes in the hippocampus and other limbic structures. Several lines of evidence suggest that reactive oxygen species (ROS) play a pivotal role in the pathogenesis of excitotoxic death by KA. Curcumin has been known to possess anti-oxidative and anti-inflammatory activities. In this study, the effects of curcumin on KA induced hippocampal cell death, reactive gliosis and biochemical changes in reactive glia were investigated by immunohistochemical methods. Our data demonstrated that curcumin attenuated KA-induced astroglial and microglial activation although it did not protect KA-induced hippocampal cell death.

• Korean Journal of Acupuncture
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• 제29권3호
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• pp.396-405
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• 2012

Objectives : To confirm whether acupuncture can suppress the degree of seizure and the activation of astrocytes in hippocampi using kainic acid(KA)-induced epilepsy mouse model. Methods : 8 weeks C57BL/6 mice(20~25 g) were given acupuncture once a day at acupoint HT8(Shaofu) bilaterally during 2 days before KA injection. After an intraperitoneal injection of 30 mg/kg KA, acupuncture treatment was subsequently administered once more(total 3 times), and the degree of seizure was observed for 120 min. The neuronal cell death, pERK expression, and astrocyte activation confirmed 1 hour and 24 hours after KA injection. Results : Acupuncture treatment at HT8 suppressed KA-induced epileptic seizure. One hour after KA injection, the pERK expression was increased, which was reduced by the acupuncture treatment. Twenty four hours after injection, the treatment decreased the KA-induced neuronal cell death, the interleukin-$1{\beta}$ expression and the astrocyte activation in the CA3 region of the mouse hippocampus. Conclusions : Acupuncture treatment at HT8 decreases the KA-induced epileptic seizure, the neural cell inflammation and death.

• Journal of Microbiology
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• 제43권2호
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• pp.213-218
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• 2005

Epilepsy constitutes a significant public health problem, and even the newest drugs and neurosurgical techniques have proven unable to cure the disease. In order to select a group of isolates which could generate an active compound with neuroprotective or antiepileptic properties, we isolated 517 actinomycete strains from soil samples taken from Jeju Island, in South Korea. We then screened these strains for possible anti-apoptotic effects against serum deprivation-induced hippocampal cell death, using the 3-(4, 5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide (MTT) assay as an in vitro test. The excitotoxic glutamate analog, kainic acid (KA), was used to induce seizures in experimental mice in our in vivo tests. As a result of this testing, we located one strain which exhibited profound neuroprotective activity. This strain was identified as a Streptomyces species, and exhibited the rifampinresistant genotype, Asn$(AAC)^$442, according to the results of 16S rRNA and rpoB gene analyses