• Journal of Biomedical Engineering Research
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• v.29 no.4
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• pp.272-277
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• 2008

Functional MRI technique was used in this study for examining the language switching mechanisms between the first language (L1) and the second language (L2). Language switching mechanism is regarded as a complex task that involves an interaction between L1 and L2. The aim of study is to find out the brain activation patterns during the phonological process of reading real English words and English words written in Korean characters in a bilingual person. Korean-English bilingual subjects were examined while they covertly read four types of words native Korean words, Korean words of a foreign origin, English words written in Korean characters, and English words. The fMRI results reveal that the left hemispheric language-related regions at the brain, such as the left inferior frontal, superior temporal, and parietal cortices, have a greater response to the presentation of English words written in Korean characters than for the other types of words, in addition, a slight difference was observed in the occipital-temporal lobe. These results suggest that a change in the brain circuitry underlying the relational processes of language switching is mainly associated with general executive processing system in the left prefrontal cortex rather than with a similarity-based processing system in the occipital-temporal lobes.

• Korean Journal of Oriental Medicine
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• v.3 no.1
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• pp.199-213
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• 1997

In convulsion state by PTZ in rat, anticonvulsive effect and some of ${\gamma}-aminobutyric$ acid(GABA)-related mechanisms of Buthus extract in brain was experimented. It was inhibited GABA-T activity, lipid peroxide generation and xanthine oxidase activity as scheduled administration in vitro and vivo. And the content of brain glutathione was increased as scheduled administration in rat. In convulsion state by PTZ of previously managed rat by Buthus extract, onset time and duration were non-specific changes but recovery time and severity was remarkably reduced. In conclusion speculated that Buthus extract inhibits convulsion by control of GABA content In brain.

• Korean Journal of Biological Psychiatry
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• v.15 no.4
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• pp.254-264
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• 2008

Objectives : The neural substrate of fear is thought to be highly conserved among species including human. The purpose of this review was to address the neural substrates of fear based on recent findings obtained from animal and human studies. Methods : Recent studies on brain regions related to fear, particularly fear conditioning in rodents and humans, were extensively reviewed. Results : This paper suggests high consistency in anatomical structure and physiological mechanisms for fear perception, response, learning and modulation in animals and humans. Conclusions : Fear is manifested and modulated by well conserved neural circuits among species interconnected with the amygdala, such as the hippocampus and the ventromedial prefrontal cortex. Further research is required to incorporate findings from animal studies into a better understanding of neural circuitry of fear in human in a translational approach.

• Molecules and Cells
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• v.37 no.7
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• pp.518-525
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• 2014

Gammaherpesvirus (${\gamma}HV$) infection of the central nervous system (CNS) has been implicated in diverse neurological diseases, and murine ${\gamma}HV$-68 (MHV-68) is known to persist in the brain after cerebral infection. The underlying molecular mechanisms of persistency of virus in the brain are poorly understood. Here, we characterized a unique pattern of MHV-68 persistent infection in neuroblastoma cells. On infection with MHV-68, both murine and human neuroblastoma cells expressed viral lytic proteins and produced virions. However, the infected cells survived productive infection and could be cultured for multiple passages without affecting their cellular growth. Latent infection as well as productive replication was established in these prolonged cultures, and lytic replication was further increased by treatment with lytic inducers. Our results provide a novel system to study persistent infection of ${\gamma}HVs$ in vitro following de novo infection and suggest application of MHV-68 as a potential gene transfer vector to the brain.

• Journal of Genetic Medicine
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• v.14 no.2
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• pp.67-70
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• 2017

Down syndrome (DS, trisomy 21) is associated with neuroanatomical abnormalities, including choroid plexus cysts and various types of brain tumors. Trisomy 21 is associated with oncogenic factor, especially in brain tumor. The brain of DS patients had a smaller volume of gray and white matter and an unbalanced cerebellum volume, indicating a smaller volume overall than normal. We report a case of a DS male patient who had an incidentally discovered neuroglial cyst in left cerebellar vermis. He visited our hospital with gait disturbance and fatigue. But, the neurologic exam was normal. To the best of our knowledge, this is the first reported case of a neuroglial cyst in a trisomy 21 patient. As the developmental mechanisms of a cyst and the choroid plexus are related, more research is needed.

• BMB Reports
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• v.46 no.6
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• pp.295-304
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• 2013

Extracellular acidification occurs not only in pathological conditions such as inflammation and brain ischemia, but also in normal physiological conditions such as synaptic transmission. Acid-sensing ion channels (ASICs) can detect a broad range of physiological pH changes during pathological and synaptic cellular activities. ASICs are voltage-independent, proton-gated cation channels widely expressed throughout the central and peripheral nervous system. Activation of ASICs is involved in pain perception, synaptic plasticity, learning and memory, fear, ischemic neuronal injury, seizure termination, neuronal degeneration, and mechanosensation. Therefore, ASICs emerge as potential therapeutic targets for manipulating pain and neurological diseases. The activity of these channels can be regulated by many factors such as lactate, $Zn^{2+}$, and Phe-Met-Arg-Phe amide (FMRFamide)-like neuropeptides by interacting with the channel's large extracellular loop. ASICs are also modulated by G protein-coupled receptors such as CB1 cannabinoid receptors and 5-$HT_2$. This review focuses on the physiological roles of ASICs and the molecular mechanisms by which these channels are regulated.

• Sleep Medicine and Psychophysiology
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• v.5 no.2
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• pp.177-184
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• 1998

Objectives : Disturbance of sleep with or without sleep apnea may impair the memory function. Sleep deficiency, sleepiness, sleep apnea and emotional problem in sleep disorders can induce an impairment of memory function. Methods : In this study, the polysomnographies were administered to 58 sleep apnea patients and 38 sleep disorder patients without sleep apnea. Their clinical symptoms were quantitatively evaluated. Short term and long term memory were evaluated before and after polysom no graphy with Digit symbol test and Rey-Osterrieth complex figure test. And correlations among various sleep, repiratory and clinical variables were statistically studied in order to explore which variables may influence on memory function. Results and Conclusions : Results are as follows. Depth of sleep cis positively correlated with memory function. As sleep apnea increases and average saturation of blood oxygen decreases, memory function is more impaired. Emotional depression, high blood pressure, obesity or alcohol impaired memory function. However, daytime sleepiness was not significantly correlated with memory function. The possible mechanisms how above factors influence on the memory function were discussed.

• Animal cells and systems
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• v.12 no.4
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• pp.211-217
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• 2008

Bax, a pro-apoptotic member of Bcl-2 family proteins, plays a central role in the mitochondria-dependent apoptosis. Apoptotic signals induce the translocation of Bax from cytosol into the mitochondria, which triggers the release of apoptogenic molecules such as cytochrome C and apoptosis-inducing factor, AIF. Bax-inhibiting peptide(BIP) is a cell permeable peptide comprised of five amino acids designed from the Bax-interaction domain of Ku70. Because BIP inhibits Bax translocation and Bax-mediated release of cytochrome C, BIP suppresses Bax-dependent apoptosis. In this study, we observed that BIP inhibited staurosporine-induced neuronal death in cultured cerebral cortex and cerebellar granule cells, but BIP failed to rescue granule cells from trophic signal deprivation-induced neuronal death, although both staurosporine-induced and trophic signal deprivation-induced neuronal death are dependent on Bax. These findings suggest that the mechanisms of the Bax activation may differ depending on the type of cell death induction, and thus BIP exhibits selective suppression of a subtype of Bax-dependent neuronal death.

• Journal of Korean Neurosurgical Society
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• v.60 no.4
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• pp.391-396
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• 2017

Objective : To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. Methods : Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. Results : GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. Conclusion : Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.

• Molecules and Cells
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• v.42 no.1
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• pp.28-35
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• 2019

Animals need to be able to alter their developmental and behavioral programs in response to changing environmental conditions. This developmental and behavioral plasticity is mainly mediated by changes in gene expression. The knowledge of the mechanisms by which environmental signals are transduced and integrated to modulate changes in sensory gene expression is limited. Exposure to ascaroside pheromone has been reported to alter the expression of a subset of putative G protein-coupled chemosensory receptor genes in the ASI chemosensory neurons of C. elegans (Kim et al., 2009; Nolan et al., 2002; Peckol et al., 1999). Here we show that ascaroside pheromone reversibly represses expression of the str-3 chemoreceptor gene in the ASI neurons. Repression of str-3 expression can be initiated only at the L1 stage, but expression is restored upon removal of ascarosides at any developmental stage. Pheromone receptors including SRBC-64/66 and SRG-36/37 are required for str-3 repression. Moreover, pheromone-mediated str-3 repression is mediated by FLP-18 neuropeptide signaling via the NPR-1 neuropeptide receptor. These results suggest that environmental signals regulate chemosensory gene expression together with internal neuropeptide signals which, in turn, modulate behavior.