• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.13-17
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• 2006

Experimentally induced cortical disorganization exhibits many anatomical features which are characteristic of cortical malformations in children with early-onset epilepsy. We used an immunocytochemical technique and extracellular field potential recordings from the dorsal hippocampus to determine whether the excitability of the CA1 pyramidal cells was enhanced in rats with exnerimentallv induced hippocampal dysplasia. Compared with control rats, the MAM-treated rats displayed a decrease of paired pulse inhibition. When $GABA_A$ receptor antagonists were blocked with $10{\mu}M$ bicuculline the amplitude of the second population spike of the MAM-treated of rats was similar to that of the first population spike, as was in the control rats. The MAM-treated rats had fewer somatostatin and parvalbumin-immunoreactive neurons than the control rats. These results suggest that the enhanced neuronal responsiveness of the in vivo recording of the CA1 in this animal model may involve a reduction of CA1 inhibition.

• Biomolecules & Therapeutics
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• v.7 no.3
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• pp.242-248
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• 1999

Diazepam, a benzodiazepine (BDZ) agonist, produces sedation and flumazenil, a BDZ antagonist, blocks these actions. The aim of this study was to examine the effects of BDZs on cortical electroencephalogram (EEG) in rats. The recording electrodes were implanted over the frontal and parietal cortices bilaterally, and the reference and ground electrodes over cerebellum under ketamine anesthesia. To assess the effects of diazepam and flumazenil, rats were injected with diazepam (1 mgHg, i.p.) and/or flumazenil ( 1 mg/kg, i.p.), and the EEG was recorded before and after drugs. Normal awake had theta peak in the spectrum and low amplitude waves, while normal sleep showed large amplitude of slow waves. The powers of delta, theta and alpha bands were increased during sleep compared with during awake. Diazepam reduced the mobility of the rat and induced sleep with intermittent fast spindles and large amplitude of slow activity, and it produced broad peak over betaL band and increased the power of gamma band, which were different from EEG patterns in normal sleep. Saline injection awakened rats and abolished fast spindles for a short period about 2-5 min from EEG pattern during diazepam-induced sleep. Flumazenil blocked both diazepam-induced sleep and decreased the slow activities of delta, theta, alpha and betaL, but not of gamma activity for about 10 min or more. This study may indicate that decrease in power of betaL and betaH bands can be used as the measure of central action of benzodiazepines, and that the EEG parameters of benzodiazepines have to be measured without control over the behavioral state by experimenter.

• Journal of Ginseng Research
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• v.24 no.3
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• pp.134-137
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• 2000

Spontaneous bursting activity was studied in rat thalamocortical slices using extracellular field potential recording to test the potential utilization of ginsenoside Rb$_1$ in controlling overactivated neural systems. In order to induce bursting activity, slices were perfused with Mg$\^$2+/-free artificial cerebrospinal fluid (ACSF). Two major types of spontaneous bursting activity, simple thalamocortical burst complexes (sTBCs) and complex thalamocortical burst complexes (cTBCs), were recorded in Mg$\^$2+/ -free ACSF. Ginsenoside Rb$_1$ selectively suppressed cTBCs. Duration and occurrence rate of cTBCs were reduced by 87.3${\pm}$10.2% and 85.3${\pm}$ 14.7% in the presence of 90 ${\mu}$M ginsenoside Rb$_1$ respectively, while amplitude and intraburst frequency were slightly changed by ginsenoside Rb$_1$. In contrast, ginsenoside Rb$_1$was much less effective in reducing duration and occurrence rate of sTBCs. We also tested effects of ginsenoside Rb$_1$ on bursting activity in the presence of a GABA$\sub$A/ receptor antagonist, bicuculline methiodide (BMI). Ginsenoside Rb$_1$ had no effect in suppressing BMI-induced bursting activities. These results suggest that ginsenoside Rbi may be useful in controlling seizure-like bursting activity under pathological conditions.

• Korean Journal of Biological Psychiatry
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• v.4 no.1
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• pp.102-107
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• 1997

Ginseng root, as a folk medicine, has been used in far eastern countries for thousands of years. Ginseng extract has been shown to have a variety of effects on the activity of the central nervous system, promoting stimulation as well as inhibition of the cortical activity. A survey of the relevant literatures has indicated that the putative anxiolytic activity of red ginseng has not been scientifically investigated. Therefore, the present study was designed to assess anxiolytic effect of gingseng total saponins(GTS). The putative anxiolytic effects of several fractions of GTS were investigated in mice using an elevated plus maze paradigm. Single dose administration of TS Fr.-I showed anxiolytic action in mice. Anxiolytic effect induced by TS Fr.-I was similar to that induced by diazepam. TS Fr.-II, TS Fr.-III and TS Fr.-IV did not show the anxiolytic action compared with that of TS Fr.-I. It was suggested that regulation of GABAergic neurotransmission may be important in the action of GTS. The Interaction of GTS fractions with benzodiazepine receptor was performed using rat cortical membranes. GTS inhibited the binding of [3H] Ro 15-1788 on the benzodiazepine receptor. Among from TS fractions, the binding activity of GTS in the TS Fr.-IV was highest, which did not show the anxiolytic activity. From these results, we conclude that GTS has anxiolytic action, and this is not related to benzodiazepine receptor binding activity.

• Animal Bioscience
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• v.37 no.8
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• pp.1345-1354
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• 2024

Objective: The objective of this study was to identify candidate genes that play important roles in skeletal muscle development in ducks. Methods: In this study, we investigated the transcriptional sequencing of embryonic pectoral muscles from two specialized lines: Liancheng white ducks (female) and Cherry valley ducks (male) hybrid Line A (LCA) and Line C (LCC) ducks. In addition, prediction of target genes for the differentially expressed mRNAs was conducted and the enriched gene ontology (GO) terms and Kyoto encyclopedia of genes and genomes signaling pathways were further analyzed. Finally, a protein-to-protein interaction network was analyzed by using the target genes to gain insights into their potential functional association. Results: A total of 1,428 differentially expressed genes (DEGs) with 762 being up-regulated genes and 666 being down-regulated genes in pectoral muscle of LCA and LCC ducks identified by RNA-seq (p<0.05). Meanwhile, 23 GO terms in the down-regulated genes and 75 GO terms in up-regulated genes were significantly enriched (p<0.05). Furthermore, the top 5 most enriched pathways were ECM-receptor interaction, fatty acid degradation, pyruvate degradation, PPAR signaling pathway, and glycolysis/gluconeogenesis. Finally, the candidate genes including integrin b3 (Itgb3), pyruvate kinase M1/2 (Pkm), insulin-like growth factor 1 (Igf1), glucose-6-phosphate isomerase (Gpi), GABA type A receptor-associated protein-like 1 (Gabarapl1), and thyroid hormone receptor beta (Thrb) showed the most expression difference, and then were selected to verification by quantitative real-time polymerase chain reaction (qRT-PCR). The result of qRT-PCR was consistent with that of transcriptome sequencing. Conclusion: This study provided information of molecular mechanisms underlying the developmental differences in skeletal muscles between specialized duck lines.

• The Journal of Korea Assosiation for Disability and Oral Health
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• v.12 no.1
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• pp.11-15
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• 2016

Angelman syndrome is characterized by a partial deficit of paired autosomal chromosome 15, which contains a subunit of the GABA (Gamma-Amino Butyric Acid) receptor. The main clinical characteristics of this syndrome are delayed neuropsychological development, intellectual disability, and speech impairment. The syndrome has oral manifestations such as diastemas, tongue thrusting, sucking swallowing disorder, and excessive chewing behavior. A 3-year-6-month old girl with Angelman syndrome was scheduled for dental treatment. She had multiple caries, but she was poorly cooperative for treatment due to developmental delay and movement disorder, so general anesthesia was considered. The patient with Angelman syndrome was successfully treated under general anesthesia. There were no postoperative complications related to anesthesia and dental treatment. When treating children with this syndrome, the dentist needs to manage their uncooperative behavior and medical problem.

• Journal of Pharmaceutical Investigation
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• v.35 no.3
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• pp.193-199
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• 2005

Gabapentin is an antiepileptic drug that is structurally similar to ${\gamma}-aminobutyric$ acid (GABA), but does not interact with the GABA receptor. It does not bind significantly to plasma proteins, and is excreted to unchanged form in the urine. The purpose of the present study was to evaluate the bioequivalence of two gabapentin capsules, $Neurontin^{TM}$ capsule 300 mg (Pfizer Pharm. Co., Ltd.) and Kuhnil $Gabapentin^{TM}$ capsule 300 mg (Kuhnil Pharm. Co., Ltd), according to the guidelines of the Korea Food and Drug Administration (KFDA). The release of gabapentin from the two gabapentin formulations in vitro was tested using KP VIII Apparatus II method with various dissolution media (pH 1.2, 4.0, 6.8 buffer solution and water). Twenty six healthy male subjects, $22.46{\pm}1.86$ years in age and $67.64{\pm}7.24$ kg in body weight, were divided into two groups and a randomized $2{\times}2$ cross-over study was employed. After a single capsule containing 300 mg as gabapentin was orally administered, blood samples were taken at predetermined time intervals and the concentrations of gabapentin in serum were determined using HPLC with fluorescence detector. The dissolution profiles of two formulations were similar at all dissolution media. In addition, the pharmacokinetic parameters such as $AUC_t$, $C_{max}$ and $T_{max}$ were calculated and ANOVA test was utilized for the statistical analysis of the parameters using logarithmically transformed $AUC_t$, $C_{max}$ and untransformed $T_{max}$. The results showed that the differences between two formulations based on the reference drug, $Neurontin^{TM}$ capsule 300 mg, were -2.03, -0.43 and 4.29% for $AUC_t$, $C_{max}$ and $T_{max}$, respectively. There were no sequence effects between two formulations in these parameters. The 90% confidence intervals using logarithmically transformed data were within the acceptance range of log 0.8 to log 1.25 $(e.g.,\;log\;0.89{\sim}log\;1.09\;and\;log\;0.91{\sim}log\;1.09$ for $AUC_t$ and $C_{max}$, respectively). Thus, the criteria of the KFDA bioequivalence guideline were satisfied, indicating Kuhnil $Gabapentin^{TM}$ capsule 300 mg was bioequivalent to $Neurontin^{TM}$ capsule 300 mg.

• Korean Journal of Clinical Laboratory Science
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• v.53 no.4
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• pp.333-341
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• 2021

Benzodiazepines (BDZs) drugs act on the GABA_A receptor, function as nerve suppressors, and are used to treat anxiety, insomnia, and panic disorder. We analyzed the data of 30 individuals to determine any differences in the sleep-electroencephalogram findings among individuals varying in age, benzodiazepine use, and duration of benzodiazepine use. Comparisons between users and non-users of benzodiazepines, short-term and long-term users, older and younger users, and older short-term and older long-term users, were achieved using electroencephalographic findings obtained through polysomnography. The parameters evaluated included sleep latency, sleep efficiency, sleep-stage percentages, number of sleep spindles, and average frequency of sleep-spindle. The difference between benzodiazepine users and non-users was significant with respect to sleep-stage percentages and average frequency of sleep-spindle. Older and younger users differed significantly with respect to sleep efficiency and sleep-stage percentages, whereas significant difference for sleep efficiency was obtained between long-term and short-term users. Taken together, our results indicate that BDZ consumption suppresses slow-wave sleep and increases the frequency of sleep spindles.

• Animal cells and systems
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• v.13 no.3
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• pp.275-281
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• 2009

The effects of pentylenetetrazol (PTZ), a GABA receptor antagonist, were studied on passive avoidance learning and expression of heat shock protein 70 (hsp70), neuroglobin, and fatty acid binding protein-7 (fabp-7) genes. Zebrafish were trained to stay in a dark compartment to avoid a weight dropping in an acryl shuttle box with a central sliding door. In two training sessions of 2 h interval, each consisting of 3 trials, the crossing time was significantly increased from $43.2{\pm}14.4s$ to $149.3{\pm}38.5s$ in the first training session and remained $116.1{\pm}36.0s$ s in the first trial of the second training session in the control. In zebrafish treated with PTZ before the first training session, the crossing time was significantly increased neither in the first nor in the second training session. However, the increased crossing time was maintained in the second training session when 10 mM PTZ was treated three times for 10 min at 30 min intervals between the first and second training session. Quantitative real-time PCR showed that expression level of hsp70 mRNA increased two to eight fold over that of control in the brain at 0-24 h after termination of PTZ treatment. No change in expression of neuroglobin and fabp-7 mRNA was shown in PTZ-treated zebrafish. Our studies suggest that PTZ impairs learning ability in avoidance response and also modifies expression of genes related to the neuroprotection.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.62-70
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• 2001

Alzheimer's disease(AD) is associated with a characteristic neuropathology. The major hallmarks of AD are senile plaques (SPs) and neurofibrillary tangles(NFTs). ${\beta}$-amyloid protein($A{\beta}$) is derived from the proteolysis of amyloid precursor protein(APP) and then converted to SPs. Mature SPs produce cytotoxicity through direct toxic effects and activation of microglia and complement. NFTs are composed of paired helical filaments(PHFs) including abnormally phosphorylated form of the microtubule-associated protein(MAP) tau and increased tau level in cerebrospinal fluid may be observed in most AD. The aggregation of $A{\beta}$ and tau formation are thought to be a final common pathway of AD. Acetylcholine, dopamine, serotonin, GABA and their receptors are associated with AD. Especially, decreased nicotinic acetylcholine receptors(nAChRs) in AD are reported. Genetic lesions associated with AD are mutations in the structural genes for the APP located on chromosome 21, presenilin(PSN)1 located on chromosome 14 and PSN2 located on chromosome 1. Also, trisomy 21, Apo-E gene located on chromosome 19, PMF locus, low density lipoprotein receptor-related protein and ${\alpha}$-macroglobulin increase risk of AD. In this article, we will review about the neurobiology of AD and some newly developed research areas.