• Title/Summary/Keyword: prefrontal cortex(PFC)

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A Neurobiological Measure of General Intelligence in the Gifted (뇌기능영상 측정법을 이용한 영재성 평가의 타당성 연구)

  • Cho, Sun-Hee;Kim, Heui-Baik;Choi, Yu-Yong;Chae, Jeong-Ho;Lee, Kun-Ho
    • Journal of Gifted/Talented Education
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    • v.15 no.2
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    • pp.101-125
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    • 2005
  • We applied functional magnetic resonance imaging (fMRI) techniques to examine whether general intelligence (g) could be assessed using a neurobiological signal of the brain. Participants were students in a national science academy and several local high schools. They were administered diverse intelligence (RAPM and WAIS) and creativity tests (TTCT-figural and TTCT-verbal). Forty of them were scanned using fMRI while performing complex and simple g tasks. In brain regions of greater blood flow in complex compared with simple g tasks, the gifted group with an exceptional g level was not significantly different from the average group with an ordinary g level: both of them activated the lateral prefrontal, anterior cingulate, posterior parietal cortices. However, the activation levels of the gifted group were greater than those of the average group, particularly in the posterior parietal cortex. Correlation analysis showed that the activity of the posterior parietal cortex has the highest correlation ($(r=0.73{\sim}0.74)$) with individual g levels and other regions also have moderate correlation ($(r=0.53{\sim}0.66)$). On the other hand, two-sample t test showed a striking contrast in intelligence tests scores between the gifted and the average group, whereas it did not show in creativity tests scores. These results suggest that it is within the bounds of possibility that a neurobiological signal of the brain is used in the assessment of the gifted and also suggest that creativity has to be given a great deal of weight on the assessment of the gifted.

Ginsenoside Rb1 attenuates methamphetamine (METH)-induced neurotoxicity through the NR2B/ERK/CREB/BDNF signalings in vitro and in vivo models

  • Yang, Genmeng;Li, Juan;Peng, Yanxia;Shen, Baoyu;Li, Yuanyuan;Liu, Liu;Wang, Chan;Xu, Yue;Lin, Shucheng;Zhang, Shuwei;Tan, Yi;Zhang, Huijie;Zeng, Xiaofeng;Li, Qi;Lu, Gang
    • Journal of Ginseng Research
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    • v.46 no.3
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    • pp.426-434
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    • 2022
  • Aim: This study investigates the effects of ginsenoside Rb1 (GsRb1) on methamphetamine (METH)-induced toxicity in SH-SY5Y neuroblastoma cells and METH-induced conditioned place preference (CPP) in adult Sprague-Dawley rats. It also examines whether GsRb1 can regulate these effects through the NR2B/ERK/CREB/BDNF signaling pathways. Methods: SH-SY5Y cells were pretreated with GsRb1 (20 mM and 40 mM) for 1 h, followed by METH treatment (2 mM) for 24 h. Rats were treated with METH (2 mg/kg) or saline on alternating days for 10 days to allow CPP to be examined. GsRb1 (5, 10, and 20 mg/kg) was injected intraperitoneally 1 h before METH or saline. Western blot was used to examine the protein expression of NR2B, ERK, P-ERK, CREB, P-CREB, and BDNF in the SH-SY5Y cells and the rats' hippocampus, nucleus accumbens (NAc), and prefrontal cortex (PFC). Results: METH dose-dependently reduced the viability of SH-SY5Y cells. Pretreatment of cells with 40 µM of GsRb1 increased cell viability and reduced the expression of METH-induced NR2B, p-ERK, p-CREB and BDNF. GsRb1 also attenuated the expression of METH CPP in a dose-dependent manner in rats. Further, GsRb1 dose-dependently reduced the expression of METH-induced NR2B, p-ERK, p-CREB, and BDNF in the PFC, hippocampus, and NAc of rats. Conclusion: GsRb1 regulated METH-induced neurotoxicity in vitro and METH-induced CPP through the NR2B/ERK/CREB/BDNF regulatory pathway. GsRb1 could be a therapeutic target for treating METH-induced neurotoxicity or METH addiction.

Effects of tianeptine on symptoms of fibromyalgia via BDNF signaling in a fibromyalgia animal model

  • Lee, Hwayoung;Im, Jiyun;Won, Hansol;Nam, Wooyoung;Kim, Young Ock;Lee, Sang Won;Lee, Sanghyun;Cho, Ik-Hyun;Kim, Hyung-Ki;Kwon, Jun-Tack;Kim, Hak-Jae
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.4
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    • pp.361-370
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    • 2017
  • Previous reports have suggested that physical and psychological stresses may trigger fibromyalgia (FM). Stress is an important risk factor in the development of depression and memory impairments. Antidepressants have been used to prevent stress-induced abnormal pain sensation. Among various antidepressants, tianeptine has been reported to be able to prevent neurodegeneration due to chronic stress and reverse decreases in hippocampal volume. To assess the possible effect of tianeptine on FM symptoms, we constructed a FM animal model induced by restraint stress with intermittent cold stress. All mice underwent nociceptive assays using electronic von Frey anesthesiometer and Hargreaves equipment. To assess the relationship between tianeptine and expression levels of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and phosphorylated cAMP response element-binding protein (p-CREB), western blotting and immunohistochemistry analyses were performed. In behavioral analysis, nociception tests showed that pain threshold was significantly decreased in the FM group compared to that in the control group. Western blot and immunohistochemical analyses of medial prefrontal cortex (mPFC) and hippocampus showed downregulation of BDNF and p-CREB proteins in the FM group compared to the control group. However, tianeptine recovered these changes in behavioral tests and protein level. Therefore, this FM animal model might be useful for investigating mechanisms linking BDNF-CREB pathway and pain. Our results suggest that tianeptine might potentially have therapeutic efficacy for FM.