xxxii Poster Presentation P-1057 P-1059 Lipocalin-2 is associated - - PDF document

xxxii

P-1057 Lipocalin-2 is associated with multiple indices of neuropathy in streptozotocin-induced diabetic mice .............................. 117

Anup Bhusal, Md Habibur Rahman, Kyoungho Suk

P-1058 Aquilariae Lignum extract attenuates glutamate-induced neuroexcitotoxicity in HT22 hippocampal cells .......................... 117

Jin-Seok Lee, Won-Yong Kim, Yoo-Jin Jeon, Sam-Keun Lee, Chang-Gue Son

P-1059 Axonal neuropathy in Charcot-Marie-Tooth disease with stop loss and translational elongations of the 3’ UTR in the neurofilament-heavy polypeptide gene .............................................................................................................................. 117

Hyun Myung Doo, Jong Hyun Kim, Soo Hyun Nam, Da Eun Nam, Ki Wha Chung, Byung-Ok Choi

Computational Neuroscience / Technology in Neuroscience P-1060 Effect of inhibitory spike-timing-dependent plasticity on burst synchronization in a scale-free neuronal network .......... 117

Sang-Yoon Kim, Woochang Lim

P-1061 Neural substrates of cognitive reserve in Alzheimer’s disease spectrum and normal aging .................................................... 118

Dong Hyuk Lee, Peter Lee, Sang Won Seo, Jee Hoon Roh, Minyoung Oh, Jungsu S. Oh, Seung Jun Oh, Jae Seung Kim, Yong Jeong

P-1062 A hierarchical neural network model for non-Hebbian dynamics of memory ensemble ......................................................... 118

Youngjin Park, Se-Bum Paik

P-1063 Universality of the developmental origins of diverse functional maps in the visual cortex .................................................... 118

Jaeson Jang, Min Song, Gwangsu Kim, Se-Bum Paik

P-1064 Long-range connections in visual cortex facilitate the integration of global visual information ........................................... 118

Seungdae Baek, Youngjin Park, Se-Bum Paik

P-1065 Fully convolutional network for human brain extraction ............................................................................................................ 119

Jinwoo Hong, Gilsoon Park, Jong-Min Lee

P-1066 Abnormal hole detection based on Hodge Laplacian .................................................................................................................... 119

Hyekyoung Lee, Moo K. Chung, Hyejin Kang, Hongyoon Choi, Yu Kyeong Kim, Dong Soo Lee

P-1067 Topographic organization of simple and complex cells in visual cortex .................................................................................... 119

Gwangsu Kim, Jaeson Jang, Se-Bum Paik

P-1068 Disrupted cortical brain network in patients with schizophrenia and bipolar disorder: a resting-state electroencephalographic study .............................................................................................................................. 119

Sungkean Kim, Yong-Wook Kim, Miseon Shim, Min Jin Jin, Chang-Hwan Im, Seung-Hwan Lee

P-1069 Anesthesia level dependent functional connectivity changes in the macaque brain ................................................................ 120

Soowon Jo, Chongwon Pae, Kyesam Jung, Junho Son, Hae-Jeong Park

P-1070 Organized state transitions in cortical brain system at rest ........................................................................................................ 120

Jiyoung Kang, Hae-Jeong Park

P-1071 Brain function and behavior ability-based correlation study for stage discrimination and monitoring of Alzheimer’s disease ........................................................................................................................................................................... 120

Jeonghwan Gwak, Cheolbin Park, Hyunsu Jeong, Sehyeon Jang, Minhee Kim, Jae Gwan Kim, Sung Chan Jun, Kyu Yeong Choi, Byeong C. Kim, Kun Ho Lee, Jong-In Song

P-1072 Translational responses of hippocampal granule cells and mossy cells to chronic antidepressant treatment ....................... 120

Jin-Hyeok Jang, Yong-Seok Oh

P-1073 Parvalbumin and somatostatin interneurons selectively modulate the propagation of asynchronous firing rates in cortical feedforward network models ........................................................................................................................................ 121

Jeongheon Gwak, Jeehyun Kwag

P-1074 aMNET: multi-modal multi-species network analysis toolbox for animal neuroimaging data ............................................... 121

Jinseok Eo, Soowon Jo, Chongwon Pae, Junho Son, Kyesam Jung, Jiyoung Kang, Hae-Jeong Park

P-1075 Subcortical white matter and grey matter brain microstructural changes in patients with alcohol dependence .................. 121

Yong-Tae Kim, Jae-Hyuk Shim, Hyeon-Man Baek

P-1076 The effect of types of the single kernels in SK-2D-GRAPPA algorithm ..................................................................................... 121

Seonyeong Shin, JungHyun Song, Inyoung Bae, Dongchan Kim, Yeji Han, Jun-Young Chung

Poster Presentation

117

Poster Presentation Forum EN Session Symposium Index Plenary Lecture Keynote Lecture Luncheon Seminar Awards P-1057

Lipocalin-2 is associated with multiple indices of neuropathy in streptozotocin-induced diabetic mice

Anup Bhusal1,2*, Md Habibur Rahman1,2*, Kyoungho Suk1,2**

1Department of Pharmacology, Brain Science & Engineering Institute, Kyungpook National

University School of Medicine, Daegu, 2Department of Biomedical Science, BK21 PLUS KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Korea

Neuropathy is a common complication of uncontrolled diabetes. Metabolic abnormalities and inflammatory process have been associated with diabetic

• neuropathy. Lipocalin-2 (LCN2) is an acute phase protein known to promote

neuroinflammation via the recruitment of inflammatory cells and the induc- tion of pro-inflammatory mediators in diverse neurological disorders. Pre- viously, our study demonstrated that LCN2 contributes to the development

• f pain hypersensitivity following peripheral nerve injury via proalgesic

chemokine expression. Here, we explore the role of LCN2 in multiple aspects

• f neuropathy in streptozotocin-induced mouse model of diabetes. In this

study, we show that induction of diabetes increased the expression of LCN2 in the multiple regions of the both central and peripheral nervous systems including hippocampus, dorsal root ganglion, and sciatic nerve. Genetic deficiency of Lcn2 in mice significantly improved diabetes-induced cogni- tive impairment, which was accompanied by the reduced glial activation in the hippocampus. Lcn2 deficiency also attenuated diabetes-induced sciatic nerve damages as determined by nerve conduction velocity and density of intra-epidermal nerve fibers. Elevated immune cells and cytokine levels in different nervous tissues were the indicative of a detrimental outcome from diabetes following LCN2 expression. Taken together, our findings highlight the critical role of LCN2 in the pathogenesis of diabetic neuropathy. Key Words: Lipocalin-2, Diabetes, Neuroinflammation, Intradermal nerve fiber density, Neuropathy P-1058

Aquilariae Lignum extract attenuates glutamate-induced neuroexcitotoxicity in HT22 hippocampal cells

Jin-Seok Lee1†, Won-Yong Kim1†, Yoo-Jin Jeon1, Sam-Keun Lee2, Chang- Gue Son1*

1Liver and Immunology Research Center, Oriental Medical Collage of Daejeon University,

Daejeon, 2Department of Applied Chemistry, Oriental Medicine Collage of Daejeon University, Daejeon, Korea

An imbalance between excitatory and inhibitory neurotransmitters is known to induce neuronal excitotoxicity which is a major cause of neu- rodegenerative disorders. Excessive glutamate concentration leads to the neuronal death by increasing oxidative stress and affecting the apoptotic signaling pathway. We investigated the anti-excitotoxic effects and asso- ciated working mechanisms of 30% ethanol extract of Aquilariae Lignum (ALE) against hippocampal neuronal death by glutamate. HT22 cells were treated with glutamate (20 mM) for 24h following pretreatment with ALE (5, 10, 25 μg/mL). Cell viability, biochemical analysis, flow chemistry, and Western blotting assays were performed. Glutamate treatment substantially increased the intracellular level of reac- tive oxygen species (ROS) and Ca2+ influx into the cell, which were fol- lowed by apoptosis. ALE pretreatment, however, significantly attenuated these excitotoxicity-related features according to the results of Annexin V analysis and the lactate dehydrogenase assay, in which the calpain pathway (in a caspase 3-independent manner) may be involved. ALE pretreatment also significantly attenuated the glutamate-induced activation of both in- flammation-associated molecules (extracellular signal-regulated kinase, c-Jun N-terminal kinases and p38) and death-related molecules (p53, apop- tosis-inducing factor). The inactivation of brain-derived neurotrophic factor (BDNF) was restored by ALE pretreatment. Our results verified that A. Lignum has potential neuroprotective effects

• n glutamate-induced excitotoxicity in hippocampal neuron cells, and its

underlying mechanism may involve the regulation of ROS-mediated cell death pathways. Key Words: Aquilariae lignum, Excitotoxicity, Calpain-dependent, Calcium

• verload, Apoptosis

P-1059

Axonal neuropathy in Charcot-Marie-Tooth disease with stop loss and translational elongations of the 3’ UTR in the neurofilament-heavy polypeptide gene

Hyun Myung Doo1, Jong Hyun Kim2, Soo Hyun Nam2, Da Eun Nam3, Ki Wha Chung3, Byung-Ok Choi1,2

1Department of Health Sciences and Technology, Samsung Advanced Institute for Health

Science & Tech., Sungkyunkwan University, Seoul, 2Department of Neurology, Stem Cell & Regenerative Medicine Institute, Samsung Medical Center, Sungkyunkwan University School

• f Medicine, Seoul, 3Department of Biological Sciences, Kongju National University, Gongju,

Korea

Previously reported a cryptic amyloidgenic element (CAE) in the 3’ UTR of the neurofilament-heavy polypeptide (NEFH) gene as the underlying cause

• f axonal Charcot-Marie-Tooth neuropathy type 2CC (CMT2CC). Two frame

shift variants (p.Asp1004Ginfs*58) and (p.Pro1008Alafs*56) in NEFH in CMT2 families result in stop loss and translation of a CAE encoded by the 3’ UTR. This study identified a de novo c.3015_3027dup predicting p.Lys- 1010Glnfs*57 in NEFH from a Korean CMT2 family with an atypical clinical symptom of prominent proximal weakness. The patient showed atypical clinical manifestations compared to the other CMT patients with axonal

• neuropathy. There was proximal weakness of the deltoid and hip muscles.

Electromyography (EMG) revealed proximal and distal chronic neurogenic changes in a non-length-dependent pattern and additional myopathic fea- tures in proximal muscles. Lower limb MRI revealed marked hyperintense signal changes in the thigh muscles compared to those in the calf mus-

• cles. In this study, we suggest that stop loss and translational elongations

by the 3’ UTR of NEFH mutations are frequent genetic cause of axonal Charcot-Marie-Tooth neuropathy harboring the characteristics of proximal dominant weakness. Key Words: Neurofilament-heavy polypeptide, NEFH, CMT2CC, Axonal neuropathy P-1060

Effect of inhibitory spike-timing-dependent plasticity on burst synchronization in a scale-free neuronal network

Sang-Yoon Kim, Woochang Lim

Institute for Computational Neuroscience and Department of Science Education, Daegu National University of Education, Daegu, Korea

We consider the Barabási-Albert scale-free network (SFN) composed of in- hibitory bursting Hindmarsh-Rose neurons. This inhibitory neuronal popu- lation has adaptive dynamic synaptic strengths governed by the inhibitory spike-timing-dependent plasticity (iSTDP). In previous works without iSTDP, burst synchronization (BS) was found to appear in a range of noise inten- sities for fixed synaptic inhibition strengths. Here, we investigate the effect

• f iSTDP on BS by varying the noise intensity. We employ an anti-Hebbian

time window for the iSTDP update rule, in contrast to the Hebbian time win- dow for the excitatory STDP. A Matthew effect in inhibitory synaptic plas- ticity is thus found to occur; good BS (with higher bursting measure) gets better via long-term depression (LTD), while bad BS (with lower bursting measure) gets worse via long-term potentiation (LTP). This kind of Matthew effect is in contrast to that in excitatory synaptic plasticity where good (bad) synchronization gets better (worse) via LTP (LTD). Furthermore, emergences

• f LTD and LTP of synaptic inhibition strengths are intensively investigated

via a microscopic method based on the distributions of time delays between the pre- and the post-synaptic burst onset times. Finally, in the presence of iSTDP we investigate the effects of network architecture on BS by varying the symmetric attachment degree $l^*$ and the asymmetry parameter $\ Delta l$ in the SFN, and Matthew effects in inhibitory synaptic plasticity are also found to occur by varying $l^*$ and $\Delta l$. Key Words: Inhibitory spike-timing-dependent plasticity, Burst synchroni- zation, Scale-free network, Bursting neurons