• The Korean Journal of Physiology and Pharmacology
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• v.13 no.2
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• pp.91-97
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• 2009

The tubby mouse is characterized by progressive retinal and cochlear degeneration and late-onset obesity. These phenotypes are caused by a loss-of-function mutation in the tub gene and are shared with several human syndromes, suggesting the importance of tubby protein in central nervous system (CNS) functioning. Although evidence suggests that tubby may act as a transcription factor mediating G-protein coupled receptor (GPCR) signaling, any downstream gene regulated by tubby has yet to be identified. To explore potential target genes of tubby with region-specific transcription patterns in the brain, we performed a microarray analysis using the cerebral cortex and hypothalamus of tubby mice. We also validated the changes of gene expression level observed with the microarray analysis using real-time RT-PCR. We found that expression of erythroid differentiation factor 1 (Erdrl) and caspase 1 (Casp1) increased, while p21-activated kinase 1 (Pak1) and cholecystokinin 2 receptor (Cck2r) expression decreased in the cerebral cortex of tubby mice. In the hypothalamic region, Casp 1 was up-regulated and $\mu$-crystallin (CRYM) was down-regulated. Based on the reported functions of the differentially expressed genes, these individual or grouped genes may account for the phenotype of tubby mice. We discussed how altered expression of genes in tubby mice might be understood as the underlying mechanism behind tubby phenotypes.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.2
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• pp.179-188
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• 2017

With the explosive increase in exposure to radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones, public concerns have grown over the last few decades with regard to the potential effects of EMF exposure on the nervous system in the brain. Many researchers have suggested that RF-EMFs can effect diverse neuronal alterations in the brain, thereby affecting neuronal functions as well as behavior. Previously, we showed that long-term exposure to 835 MHz RF-EMF induces autophagy in the mice brain. In this study, we explore whether shortterm exposure to RF-EMF leads to the autophagy pathway in the cerebral cortex and brainstem at 835 MHz with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Increased levels of autophagy genes and proteins such as LC3B-II and Beclin1 were demonstrated and the accumulation of autophagosomes and autolysosomes was observed in cortical neurons whereas apoptosis pathways were up-regulated in the brainstem but not in the cortex following 4 weeks of RF exposure. Taken together, the present study indicates that monthly exposure to RF-EMF induces autophagy in the cerebral cortex and suggests that autophagic degradation in cortical neurons against a stress of 835 MHz RF during 4 weeks could correspond to adaptation to the RF stress environment. However, activation of apoptosis rather than autophagy in the brainstem is suggesting the differential responses to the RF-EMF stresses in the brain system.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.83.1-83.1
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• 2003

The heterotrimeric G protein subunits (G ) are region-specifically expressed in brain such as hypothalamus and pituitary gland in abundant, suggesting that is may be associated with “stress-axis”. This study was designed to examine the effect of stress on the region-specific expression of various G subunits in rat brain. The localization of mRNAs encoding seven of G and striking region-specific patterns of expression were observed in 12 different regions of both non-stressed and stressed rat brain; (1) frontal cortex area, (2) cerebral cortex area, (3) striatum, (4) hippocampus area, (5) thalamus, (6) brain stem, (7) cerebellum area, (8) hypothalamus, (9) septum, (10) amygdala, (11) preoptic area, and (12) pituitary gland. (omitted)

• Physical Therapy Rehabilitation Science
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• v.11 no.4
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• pp.571-578
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• 2022

Objective: Cognitive-motor trainings had a positive impact on cognitive function and dual-task trainings led to improvements of global cognitive function. The brain activity of the prefrontal cortex (PFC) is another indicator that can infer cognitive function. This study aims to confirm the usability of the interactive system cognitive-motor training program and the changes in the prefrontal cortex through training. Design: Cross-sectional study Methods: In this study, two cognitive tasks were randomly applied to 20 adults as cognitive-motor training using an interactive system, and the same task was performed using the original method. During all tasks, the brain activity of the prefrontal cortex was measured by the change in oxyhemoglobin (HbO) in real-time using Functional Near-Infrastructure. After performing the tasks, the usability of the developed interactive system was evaluated by a usability questionnaire which consists of five items, and each item consists of a 7-point Likert scale that responds from 1 point to 7 points. Results: The HbO levels were increased during cognitive task performance than at the resting phase. And evaluating the usefulness of the interactive system, a questionnaire result showed that it would be useful for cognitive-motor programs. Conclusions: The cognitive-motor training using the interactive system increased the activity of the prefrontal cortex, and the developed wearable sensor-based interactive system confirmed its usefulness.

• Investigative Magnetic Resonance Imaging
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• v.26 no.2
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• pp.96-103
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• 2022

Purpose: The survival of organisms critically depends on avoidance responses to life-threatening stimuli. Information about dangerous situations needs to be remembered to produce defensive behavior. To investigate underlying brain regions to process information of danger, manganese-enhanced MRI (MEMRI) was used in olfactory fear-conditioned rats. Materials and Methods: Fear conditioning was conducted in male Sprague-Dawley rats. The animals received nasal injections of manganese chloride solution to monitor brain activation for olfactory information processing. Twenty-four hours after manganese injection, rats were exposed to electric foot shocks with odor cue for one hour. Control rats were exposed to the same odor cue without foot shocks. Forty-eight hours after the conditioning, rats were anesthetized and their brains were scanned with 9.4T MRI. Acquired images were processed and statistical analyses were performed using AFNI. Results: Manganese injection enhanced brain areas involved in olfactory information pathways in T1 weighted images. Rats that received foot shocks showed higher brain activation in the central nucleus of the amygdala, septum, primary motor cortex, and preoptic area. In contrast, control rats displayed greater signals in the orbital cortex and nucleus accumbens. Conclusion: Nasal delivery of manganese solution enhanced olfactory signal pathways in rats. Odor cue paired with foot shocks activated amygdala, the central brain region in fear, and related brain circuits. Use of MEMRI in fear conditioning provides a reliable monitoring technique of brain activation for fear learning.

• Korean Journal of Biological Psychiatry
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• v.22 no.3
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• pp.109-112
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• 2015

Since the early 2000s, there has been a continued interest in lie detection using functional magnetic resonance imaging (fMRI) in neuroscience and forensic sciences, as well as in newly emerging fields including neuroethics and neurolaw. Related fMRI studies have revealed converging evidence that brain regions including the prefrontal cortex, anterior cingulate cortex, parietal cortex, and anterior insula are associated with deceptive behavior. However, fMRI-based lie detection has thus far not been generally accepted as evidence in court, as methodological shortcomings, generalizability issues, and ethical and legal concerns are yet to be resolved. In the present review, we aim to illustrate these achievements and limitations of fMRI-based lie detection.

• YAKHAK HOEJI
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• v.34 no.5
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• pp.323-333
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• 1990

To study influence of carbonmonoxide (CO) poisoning on the content of amino acid neurotransmitter in brain, male rat was exposed to CO 5000 ppm for 30 minutes (60-75% HbCO). Aspartic acid and glutamic acid level in the cerebral cortex and aspartic acid level in the striatum were significantly decreased. GABA level in the cerebral cortex was significantly increased after the 30 and 60 minutes of CO intoxication. Taurine level in both the cerebral cortex and the striatum was increased although nonsignificant. Consequently, the CO-induced hypoxia brain showed lower level of excitatory neurotransmitter, aspartic acid and glutamic acid and higher level of inhibitory neurotransmitter, GABA and taurine. These results suggest that the change in content of amino acid neurotransmitter in the rat brain may be concerned with several CO poisoning symptoms.

• Molecules and Cells
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• v.37 no.7
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• pp.554-561
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• 2014

Lysophosphatidic acid (LPA) is a lipid growth factor that exerts diverse biological effects through its cognate receptors ($LPA_1-LPA_6$). $LPA_1$, which is predominantly expressed in the brain, plays a pivotal role in brain development. However, the role of $LPA_1$ in neuronal migration has not yet been fully elucidated. Here, we delivered $LPA_1$ to mouse cerebral cortex using in utero electroporation. We demonstrated that neuronal migration in the cerebral cortex was not affected by the overexpression of $LPA_1$. Moreover, these results can be applied to the identification of the localization of $LPA_1$. The subcellular localization of $LPA_1$ was endogenously present in the perinuclear area, and overexpressed $LPA_1$ was located in the plasma membrane. Furthermore, $LPA_1$ in developing mouse cerebral cortex was mainly expressed in the ventricular zone and the cortical plate. In summary, the overexpression of $LPA_1$ did not affect neuronal migration, and the protein expression of $LPA_1$ was mainly located in the ventricular zone and cortical plate within the developing mouse cerebral cortex. These studies have provided information on the role of $LPA_1$ in brain development and on the technical advantages of in utero electroporation.

• Journal of radiological science and technology
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• v.34 no.1
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• pp.17-25
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• 2011

In this study, we examined the impact caused by chronic exposure to Mn by investigating the degree of brain activation based on the data of recognition activities using fMRI (functional magnetic resonance imaging). A questionnaire survey, blood tests, and fMRI tests were carried out with respect to two groups. Group 1 was an exposure group consisting of 15 male workers who are 34 years old or older, and who worked for longer than 10 years in a shipbuilding factory as a welder. Group 2 was a control group consisting of 15 workers in manufacturing industries with the same gender and age. The results showed that blood Mn concentration of Group 1($1.3\;{\mu}g/dl$) was significantly higher than that of Group 2($0.8\;{\mu}g/dl$)(p < 0.001), and Pallidal Index (PI) of Group 1 was also significantly higher than that of Group 2 (p < 0.001). PI value of the group whose blood Mn concentration was $0.93\;{\mu}g/dl$ or higher was significantly higher than that of the group whose blood Mn concentration was less than $0.93 \;{\mu}g/dl$ (p < 0.001). As for brain activity area within the control group, the right and the left areas of occipital cortex showed significant activity and the left area of middle temporal cortex, the right area of superior inferior frontal cortex and inferior parietal cortex showed significant activity. Unlike the control group, the exposure group showed significant activity on the right area of superior inferior temporal cortex, the left of insula area. In the comparison of brain activity areas between the two groups, the exposure group showed significantly higher activation than the control group in such areas as the right inferior temporal cortex, the left area of superior parietal cortex and occipital cortex, and cerebellum including middle temporal cortex. However, in nowhere the control group showed more activated area than the exposure group. As the final outcome, chronic exposure to Mn increased brain activity during implementation of arithmetic task. In an identical task, activation increased in superior inferior temporal cortex, and insula area. And it was discovered that brain activity increase in temporal area and occipital area was more pronounced in the exposure group than in the control group. This result suggests that chronic exposure to Mn in the work environment affects brain activation neuro-network.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.1-8
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• 2016

Damage in the periphery or spinal cord induces maladaptive plastic changes along the somatosensory nervous system from the periphery to the cortex, often leading to chronic pain. Although the role of neural circuit remodeling and structural synaptic plasticity in the 'pain matrix' cortices in chronic pain has been thought as a secondary epiphenomenon to altered nociceptive signaling in the spinal cord, progress in whole brain imaging studies on human patients and animal models has suggested a possibility that plastic changes in cortical neural circuits may actively contribute to chronic pain symptoms. Furthermore, recent development in two-photon microscopy and fluorescence labeling techniques have enabled us to longitudinally trace the structural and functional changes in local circuits, single neurons and even individual synapses in the brain of living animals. These technical advances has started to reveal that cortical structural remodeling following tissue or nerve damage could rapidly occur within days, which are temporally correlated with functional plasticity of cortical circuits as well as the development and maintenance of chronic pain behavior, thereby modifying the previous concept that it takes much longer periods (e.g. months or years). In this review, we discuss the relation of neural circuit plasticity in the 'pain matrix' cortices, such as the anterior cingulate cortex, prefrontal cortex and primary somatosensory cortex, with chronic pain. We also introduce how to apply long-term in vivo two-photon imaging approaches for the study of pathophysiological mechanisms of chronic pain.