その他 Others
P3-1-186 環境音刺激と空間イメージとの組合わせに対する主観的評価から生じる適合感に関する生体反応計測 Physiological responses that induced by making fit selection in subjective evaluation using sound stimulation evoked spatial size image ○首藤文洋1,2, 杉本皓司2, 柿崎美智子2, 山下賢也2, 戸嶋知春3, 久野節二1,2 ○Fumihiro Shutoh1,2, Koji Sugimoto2, Michiko Kakizaki2, Kenya Yamashita2, Chiharu Toshima3, Setsuji Hisano1,2 筑波大学医学医療系1, 筑波大学大学院人間総合科学研究科感性認知脳科学専攻2, 筑波大学生命環境学群生物学類3 Faculty of Medicine, Univ of Tsukuba, Tsukuba, Japan1, Maj Kansei Behavioral and Brain Sciences, Grad Sch Compreh Hum Sci, Univ Tsukuba2, Coll Biol Sci, Sch Life Env Sci, Univ Tsukuba3 Perception of environmental sensory stimuli through sounds, odors, foods or air conditions induces several kinds of emotions, despite the underlying biological mechanism is still unclear. To explore the mechanisms of human emotion, experimental data from subjective methods provide a lot of useful data. But these data always contain risks of incorrectness when outputting participants' evaluation on answer materials. In this study, we tried to find physiological features when participants fit their emotional images to an answer material. Hearing experience actually evokes emotional response on the human. When people hear sound or music, they must be evoked spatial image of the situation where fit to the evoked emotion. Then, we examined participants' brain and autonomic nerve response during exposure to sound stimulation and fitting spatial image size that evoked by the sound stimulation. Briefly, participants were exposed several kinds of sounds, which were selected from nature, living environment and music. A schematic picture of landscape was projected in front of them. Participants controlled a slider to change angular field of the landscape picture by zooming until they fell the angular have fit to their evoked spatial image. During the experiment, we recorded several physiological data (optical topography, skin conductance, heart beat rate and skin surface temperature) from participant. Position of the zooming slider was also recorded. Then, we analyzed a correlation between motion of the slider and physiological response of the participant. This present method can provide objective evidence to subjective evaluation based on the human emotion.	P3-1-187 マウスにおける Usp46 変異が GABAA 受容体サブユニットに及ぼす影響 Ubiquitin-specific peptidase 46 (Usp46) regulated GABAA receptor subunits in the mouse brain ○今井早希1, 海老原史樹文1 ○Saki Imai1, Shizufmi Ebihara1 名古屋大院・生命農1 Bioagri, Univ of Nagoya, Aichi1 We have previously identified ubiquitin-specific peptidase 46 (Usp46) as a quantitative trait gene responsible for decreasing TST (tail suspension test) and FST (forced swimming test) immobility time in mice. This Usp46 mutation has a 3-bp deletion coding for lysine in the open reading frame, and we demonstrated that Usp46 is implicated in the regulation of the GABAergic system (Nature Genetics, 2009). The 3-bp deleted Usp46 (MT) and Usp46 KO mice showed an increase in TST immobility time by an administration of nitrazepam (an agonist at the benzodiazepine-binding site of the GABAA receptor, which potentiates the action of GABA), and the effects of nitrazepam were antagonized by flumazenil, indicating that the GABAA receptor participates in the regulation of TST immobility time. In order to understand how far Usp46 controls behavioral phenotypes, we subjected Usp46 MT and KO mice to multiple behavioral tests, including the open field test, ethanol preference test, ethanol-induced loss of righting reflex test, sucrose preference test, novelty-suppressed feeding test, marble burying test, and novel object recognition test. Although behavioral phenotypes of the Usp46 MT and KO mice were not always identical, deficiency of Usp46 significantly affected performance in all these tests. To understand the underlying mechanisms of these behaviors, we examined expression levels of GABAA receptor subunits in Usp46 mutant and KO mice by the western blotting assay and found that protein expression of several GABAA receptor subunits are altered in several brain regions where Usp46 is expressed. These results suggest that behavioral alterations in Usp46 deficient mice might be due to defective functions of GABAA receptors, although further studies are required to prove.
P3-1-188 抽象絵画鑑賞時における画家・素人の注視パターン Fixation patterns of artists and laymen during observation of abstract paintings ○小出真子1, 久保孝富1, 柴田智広1, 池田和司1 ○Naoko Koide1, Takatomi Kubo1, Tomohiro Shibata1, Kazushi Ikeda1 奈良先端科学技術大学院大学 情報科学研究科1 Graduate School of Information Science, Nara Institute of Science and Technology, Nara1 It has been known that artists have a different distribution of saccadic distances from that of laymen in painting observation. This may be caused by the difference of fixation distributions between artists and laymen although this fact does not fit easily the theory of saliency map suggesting fixation distributions are generally predictable from given visual stimulus. This map represents attention to early salient features like a high contrast of hue. Another possible cause of the difference is the time dependency of the distribution. In fact, a skilled reader with high capacity of working memory fixates on a word with fewer repetitions. To analyze the difference of the fixation distributions between artists and laymen quantitatively, we compared the distributions in two points: One is the correlation coefficient (CC) between the fixation distribution and the saliency map for a painting and the other is the autocorrelation (AC) of the fixation points as a time-series. Five artists and six laymen participated in the experiment where they were asked to observe 20 abstract paintings for 20 seconds respectively. During the observation, their fixation points were recorded at 500 Hz and processed into a fixation distribution using a kernel density function. As a result, the artists had significantly lower CCs than the laymen although their ACs were not significantly different. Our results suggest an artist attends something different from salient features but it is still unknown. In addition, our experiments could not elucidate the time dependency of the fixation distribution as seen in reading.	P3-1-189 脳室内ストレプトゾトシン注入ラットの空間認知機能障害とインスリン投与の効果 Cognitive impairments in intraventricularly streptozotocin-injected rats and effects of insulin administration ○鬼頭昭三1, 新郷明子2, 村勢敏郎2 ○Shozo Kito1, Akiko Shingo2, Toshio Murase2 茅ヶ崎徳洲会クリニック1, 冲中記念成人病研究所2 Chigasaki Tokushu-kai Clinic, Kanagawa, Japan1, Okinaka Memorial Institute for Medical Research, Tokyo, Japan2 Recently, it has been pointed out that diabetic patients have impaired learning/memory, and 3- to 4-fold increased risk of dementia. Mechanisms that are underlying diabetic cognitive dysfunction are left for studies. It is assumed that there will be impairments of insulin signaling within the brain, especially in the hippocampus. The present study was performed to elucidate the mechanism of diabetic cognitive disorders. Rats in which 80 mg/kg streptozotocin was intraventricularly injected (brain diabetes rats) were prepared. On the rats, cue and place navigation tasks were imposed with use of Morris water maze measuring the total swimming distance, total swimming time, time needed to reach the platform and path efficiency. The "brain diabetes rats" showed elongations in all of these parameters compared to control rats. One shot intraventricular injection of the long acting insulin, detemir brought about marked improvements in results of the behavioral experiments. These results indicate that the insulin analogue might bring beneficial effects on cognitive impairments including Alzheimer type dementia.
P3-1-190 脳室内インスリン・アナログの投与はストレプトゾトシン脳室内投与ラットの海馬変化を回復する―形態学的研究 The intracerebral administration of insulin analogue recovers STZ-induced morphological changes in the hippocampus ○新郷明子1, 鬼頭昭三2, 村勢敏郎1 ○Akiko Shingo1, Shozo Kito2, Toshio Murase1 冲中記念成人病研究所1, 茅ヶ崎徳洲会クリニック2 Okinaka Mem Inst for Med Res, Tokyo, Japan1, Chigasaki Tokushu-kai Clinic, Kanagawa, Japan2 Recently, it has been pointed out that diabetic patients have impaired learning/memory and 3- to 4-fold increased risk of dementia. Mechanisms that are underlying diabetic cognitive dysfunction are left for studies. It is assumed that there will be impairments of insulin signaling within the brain, especially in the hippocampus. The present study was undertaken to examine effects of intraventricular injection of an insulin analogue on the hippocampal morphological changes of intraventricularly streptozotocin injected rats (STZ-3V-rats). We administrated a long-acting insulin analogue, detemir, into the third ventricle of the STZ-3V- rats and assessed hippocampal immunohistochemistry and Golgi-Cox staining. Detemir treatment resulted in increases in IDE, insulin receptor, Akt, somatostatin, and a marked decrease of amyloid beta protein in the hippocampus reversing the streptozotocin -induced immunohistochemical changes in the STZ-3V-rats. The streptozotocin-induced decrease of granule cell layer neurons was also recovered by insulin administration. These results indicate a strong resemblance between 'brain diabetes' and human Alzheimer-type dementia, and suggest that insulin analogues may be promising therapeutic agents to attenuate cognitive decline.	P3-1-191 恐怖記憶形成におけるSlitrk4の役割 An essential role of Slitrk4 in the establishment of fear memory controlling neural circuit in amygdala ○松本圭史1, 三輪秀樹2,4, 片山圭一1, 山田一之3, 小田川摩耶1, 野崎弥生1, 柳川右千夫2,4, 有賀純1 ○Yoshifumi Matsumoto1, Hideki Miwa2,4, Kei-ichi Katayama1, Kazuyuki Yamada3, Maya Odagawa1, Yayoi Nozaki1, Yuchio Yanagawa2,4, Jun Aruga1 理化学研究所 脳科学総合研究センター 行動発達障害研究チーム1, 群馬大学大学院医学系研究科　脳神経発達統御学講座　遺伝発達行動学分野2, 理化学研究所 脳科学総合研究センター　動物資源開発支援ユニット3 Laboratory for Behavioral and Developmental Disorders, RIKEN Brain Science Institute (BSI), Wako-shi, Saitama, Japan1, Department of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan2, Support Unit for Animal Experiments, RIKEN Brain Science Institute (BSI), Wako-shi, Saitama, Japan3, JST, CREST, Tokyo, Japan4 Slitrks are neuronal transmembrane proteins that have been implicated in the pathogenesis of several neurological disorders. A member of mouse Slitrk family, Slitrk4 is strongly expressed in several brain regions such as amygdala and cortex. To clarify the physiological role of Slitrk4, we developed and characterized Slitrk4-knockout mice. Although Slitrk4 deficient mice developed normally without any obvious changes in their external appearances, they showed intriguing abnormalities in behavioral tests. Particularly of note was the elevated fear memory in cued test of classical fear conditioning without obvious alterations in the context test. To examine the activities of thalamo-amygdala afferent neurons, we performed electrophysiological analysis. Slitrk4-deficient mice showed enhanced long-term potentiation (LTP) in thalamo-amygdala afferent in the absence of GABA(A) receptor antagonist picrotoxin, but not in the presence of picrotoxin, suggesting the defective GABAergic neurotransmission. Accordingly, a subset of GABAergic interneurons was decreased in a lateral amygdala region of Slitrk4-deficient mice. It was considered that reduction of the interneurons in the lateral amygdala underlies the elevated fear memory in Slitrk4-deficient mice. These results corroborate the essential role of Slitrk4 in higher brain functions and warrant further investigation of its molecular function and possible involvement in the pathophysiology of post-traumatic stress disorders.
P3-1-192 抗うつ薬によって引き起こされる成体マウス前頭皮質内側部の脱成熟 Neuronal dematuration induced by antidepressant treatment in medial frontal cortex of adult mice ○大平耕司1,2, 竹内理香1,2, 宮川剛1,2,3 ○Koji Ohira1,2, Rika Takeuchi1,2, Tsuyoshi Miyakawa1,2,3 藤田保衛大・総医研・システム医1, 生理研・行動代謝セ・行動様式3 Divi Sys Med Sci, ICMS, Fujita Hlth Univ, Toyoake, Japan.1, CREST, JST, Kawaguchi, Japan.2, Sec Behav Patterns, Center Gen Anal Behav, NIPS, Okazaki, Japan.3 Fluoxetine (FLX), an antidepressant drug, has been widely used to treat depression and anxiety disorders. Although cellular mechanisms underlying the antidepressant effect of FLX remain largely unknown, FLX has been known to have various effects on brains, such as increased adult neurogenesis in hippocampus and cortex, dematuration of hippocampal granule cells and amygdala neurons However, it is not clear whether FLX has dematuration effect on neurons in the adult cortex. In this study, using immunohistological analysis, we studied the dematuration effect of FLX on neurons in the medial frontal cortex (mFC) of adult mice. Focusing on perineuronal nets (PNNs), an extracellular matrix, which are components of mature neurons, we found that FLX treatment decreases the number of PNN and parvalbumin double-positive interneurons. The immunoreactivity of PSA-NCAM, which is a marker for immature neurons, was remarkably increased in the mFC by FLX treatment, compared to vehicle treatment. These results suggest that FLX may convert parvalbumin-positive interneurons to an pseudo-immature state in the mFC. The potential relevance of the dematuration of interneurons in the mFC to the therapeutic or side effect of FLX on depression will be discussed.	P3-1-193 ホームケージ活動性に関わるQTLクラスターの遺伝的解析 Genetic dissection of clustered QTLs related to strain difference of home-cage activity ○小出剛1,2, 石井亜矢子1, 西明紀1, 梅森十三1, 栗木哲3, 加藤昇吾3 ○Tsuyoshi Koide1,2, Ayako Ishii1, Akinori Nishi1, Juzoh Umemori1, Satoshi Kuriki3, Shogo Kato3 国立遺伝学研究所1, 総研大2, 統計数理研究所3 Mouse Genomics Resource Laboratory, National Institute of Genetics1, SOKENDAI2, The Institute of Statistical Mathematics3 Wild-derived mouse strains exhibit large variation of home-cage activity among strains. The aim of this study is to elucidate the genetic basis of strain difference in home-cage activity. The wild-derived mouse strain MSM/Ms (MSM) exhibits higher activity in the home-cage than C57BL/6 (B6), a commonly used laboratory strain. We have analyzed consomic strains derived from B6 and MSM to elucidate genetic mechanism responsible for strain differences in the regulation of home-cage activity. Nearly half of the consomic strains showed significant difference in home-cage activity compared to B6. In order to identify a causative gene related to different level of home-cage activity, we focused on one of the chromosomes, Chr6, which shows low level of activity. A QTL analysis as well as further sub-consomic studies revealed that at least four loci are clustered in 14.5 Mbp chromosomal region. Among these loci, one locus increases activity and three others reduce activity. Our study showed that QTL can be dissociated into more loci with different effects on the phenotype. Thus, the results illustrated complex nature of genetic basis for complex traits.
P3-1-194 Hippocampal dysfunctions in tumor-bearing mice ○Changjong Moon1, Miyoung Yang1,4, Juhwan Kim1, Jong-Choon Kim1, Sung-Ho Kim1, Joong-Sun Kim2, Taekyun Shin3, Hongbing Wang4 Department of Veterinary Anatomy, College of Veterinary Medicine, Chonnam National University, Gwangju, South Korea1, Research center, Dongnam institute of Radiological & Medical Sciences (DIRAMS), Busan, South Korea2, Department of Veterinary Anatomy, College of Veterinary Medicine, Jeju National University, Jeju, South Korea3, Department of Physiology and Neuroscience Program, Michigan State University, USA4 Individuals suffering from cancer are especially susceptible to depression and cognitive difficulties. However, the precise mechanisms underlying cancer-induced brain dysfunction are poorly understood. The present study investigated the effects of cancer itself on the hippocampus-dependent behaviors and the related mechanisms in adult BALB/c mice inoculated with colon carcinoma cell line (CT26). CT26-inoculated mice showed significant impairments of hippocampus-dependent behaviors, including depression-like behavior (in tail suspension test) and memory deficit (in object recognition memory) 2 weeks after inoculation, compared to saline-inoculated controls. The tumor-bearing mice showed significant decrease in the number of doublecortin (an immunohistochemical marker for immature progenitor neurons)-positive cells in the hippocampus. The peripheral tumor remarkably altered the levels of inflammatory cytokines (e.g., interleukin-6 and -10, interferon-gamma, and tumor necrosis factor-alpha) in the plasma and hippocampus, and the stress-related parameters (e.g., plasma corticosterone and weight of adrenal glands). Therefore, the peripheral tumor alone might be sufficient to induce the hippocampus-related behavioral dysfunctions, possibly through the alterations of immune and endocrine system.	P3-1-195 Sleep deprivation-induced short-term memory deficit is preventable ○Sih-Ting Lin1, Lukas Jyuhn-Hsiarn Lee2,3, Li-Jen Lee1,4,5 Graduate Institute of Anatomy and Cell Biology, National Taiwan University1, Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Miaoli, Taiwan2, Institute of Brain and Mind Sciences National Taiwan University, Taipei, Taiwan3, Neurobiology and Cognitive Science Center, National Taiwan University, Taipei, Taiwan4 In our daily life, sleep disturbance or deprivations are inevitable. However, it is well documented that sleep loss impairs cognitive functions such as learning and memory. Reductions of neurotrophic factors, such as BDNF, subsequent to sleep deprivation have been proposed to be the key. In this study, we tested if voluntary exercise, a well known practice that increases the BDNF level, can prevent sleep loss-caused cognitive decline. Adolescent male mice were assigned into control and exercise groups. Mice in exercise group were allowed for voluntary exercise on running wheels for four weeks. Two groups of mice were then subjected to normal sleep or 72-hour sleep deprivation conditions. The locomotor activity of mice was then measured and a novel object recognition test was used to evaluate their short-term memory function. The activity level was not affected by either exercise or sleep deprivation. The performance of short-term memory was impaired in sleep-deprived control mice but not in exercised mice. Our results demonstrated a preventive effect of voluntary exercise on 3-day sleep loss-produced short-term memory deficit. To elucidate the underlying mechanism, further study is required.
P3-1-196 A dynamic factor analysis model for exploring functional connectivity revealed by resting state NIRS data ○Chung-Ping Cheng1,2, Hsin-Chin Chen2, Ching-Feng Huang3 National Cheng Kung University1, National Chung Cheng University2 Near-infrared spectroscopy (NIRS) is a noninvasive method to study neural activity by recording the concentration change of oxy-hemoglobin and deoxy-hemoglobin in the brain tissue. Several studies suggested an exploration of functional connectivity by analyzing resting-state NIRS data. But most methods devoted in the above issue ignored series dependence of the NIRS data, and assumed vixels are influenced by only one cognitive function.The study modified dynamic factor analysis (DFA) model in Browne & Nesselroade (2005) to analyze resting-state NIRS data. DFA can be considered as a method for factor analysis of multiple time series. Similar to ordinal factor analysis, observed variables in DFA may load in more than one factor and contain measurement errors. Comparable with time series analysis, serial dependence in the data is taken into account in DFA. In this study, we extended DFA to explain the cross-lagged influence from the given factor to observed variables as well as the cross-lagged influence between the latent factors. Parameter estimation and model evaluation are conducted by converting the proposed model to structural equation models. Adequacy of the proposed model is thus evaluated by artificial and real NIRS data sets.

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