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P2-2-143 味刺激により誘発される口球筋活動パターンに対する産卵ホルモンの効果 Effects of egg-laying hormone on the activity patterns of buccal muscles that were induced by taste stimulation ○成末憲治1, 長濱辰文1 ○Kenji Narusuye1, Tatsumi Nagahama1 東邦大・薬・生物物理1 Dept. Biophys., Fac. Pharmaceut. Sci., Toho univ., Chiba, Japan1 Egg-laying behavior in Aplysia is accompanied by behavioral changes such as feeding suppression. We previously showed that injection of egg-laying hormone (ELH) into the body cavity inhibited the intake of seaweed and ELH applied to the buccal ganglia increased the firing activity of jaw-closing motor neuron [JC2] during the rhythmic feeding-like responses. Feeding motor programs in Aplysia kurodai can take the form of both preferred ingestion-like responses and non-preferred rejection-like responses. It is possible that the suppressive effect of ELH on food intake is associated with a reduction of the preferred ingestion-like responses and/or an increase of the non-preferred rejection-like responses. The activity patterns in the different portions (ma and mm) of the intrinsic buccal muscles I1 + I3 differed during the 2 types of responses. In this study, we performed extracellular recordings in the ma and mm portions of the buccal muscles to determine the feeding-related responses during ELH application in the semi-intact preparations. The rhythmic burst activity in both muscle portions and the rhythmic movements of the jaws were induced after the taste stimulation (Undaria pinnatifida) to the lips. After ELH application, the ingestion-like burst numbers were significantly decreased, while the rejection-like burst numbers were significantly increased in comparison with the control. These results suggest that ELH-induced feeding suppression is associated not only with a reduction of the fraction of preferred ingestion-like responses, but also with an increase of the non-preferred rejection-like responses.	P2-2-144 身体疲労の評価に関わる神経基盤：脳磁図を用いて Neural substrates related to physical fatigue sensation for the evaluation of ourselves: a magnetoencephalography study ○石井聡1, 田中雅彰1, 山野恵美1, 渡辺恭良1,2 ○Akira Ishii1, Masaaki Tanaka1, Emi Yamano1, Yasuyoshi Watanabe1,2 大阪市立大学1, 理化学研究所分子イメージング科学研究センター2 Department of Physiology, Osaka City University Graduate School of Medicine1, RIKEN Center for Molecular Imaging Science2 There have been several studies related to the neural mechanisms of fatigue sensation. However, the neural mechanisms of fatigue sensation as for the evaluation of ourselves had not been studied. In this study, we tried to identify the neural substrates evoked when participants evaluated their subjective levels of physical fatigue. We used magnetoencephalography (MEG) with high temporal resolution to measure the neural activities. Ten healthy participants were enrolled in our study. This study was approved by the Ethics Committee of Osaka City University, and all the participants gave written informed consent for participation. All the participants were right-handed. During MEG recordings, they were asked to evaluate their subjective levels of physical fatigue of the right hand in time with execution cues (evaluation session) or only to pay attention to their right hand in time with execution cues (control session). In the evaluation session, equivalent current dipoles (ECDs) with mean latencies approximately 380 ms were observed in 9 of 10 participants, which were localized in the posterior cingulate cortex (PCC), while in the control session, the ECDs in that brain region was observed in 2 of 10 participants. The proportion of the participants in whom ECDs in the PCC were observed in the execution session was statistically higher than that in the control session (P < 0.05, McNemar test). In addition, the intensities of the ECDs were positively associated with the extent to which participants considered to successfully evaluate the fatigue of their right hand (r = 0.663, P = 0.036) in the evaluation session. These data suggest that the PCC is involved in the neural substrates related to the physical fatigue sensation to evaluate ourselves.
P2-2-145 2型糖尿病モデルマウスでの運動開始週齢と運動強度によるオレキシン神経活性の比較 Exercise induced activation of orexin neurons depends on the stage of illness and exercise intensity in type 2 diabetes mellitus model mice ○細江さよ子1, 仙波恵美子1 ○Sayoko Hosoe1, Emiko Senba1 和歌山県立医科大学医学部　大学院医学研究科　第二解剖1 Dept. Anat. and Neurobiol., Wakayama Med. Univ.1 Physical exercise is recommended for the prevention and treatment of type 2 diabetes. Hypothalamic orexin (ORX) neurons play key roles in the autonomic control during exercise. We examined the effects of exercise on the activity of ORX neurons in db/db mice as a model of type 2 diabetes, and m/db mice as control. Both of them were divided into 2 groups; treadmill running exercise (E) and sedentary (S) groups. The exercise groups were further divided into 2 groups; low intensity exercise (LE) and high intensity exercise (HE) groups. Exercise protocol of LE consisted of 7m/min x45 min/day for 4 weeks, and that of HE consisted of 45 min running with gradual increase in intensity from 7m/min (week 1) to 15m/min (week 4). In our previous study, we found that ORX neurons in the hypothalamus was activated by LE in m/db and db/db mice and by HE in m/db mice, but not by HE in db/db mice when the exercise started at 12 week-old (12W-). In the present study, we started the exercise training at 8 week-old (8W-) and examined the effect on the activation of hypothalamic neurons. C-fos immunoreactivity (IR) in ORX neurons was quantified by double immunofluorescence with anti c-fos and anti ORX-A antibodies. C-fos-positive neurons were also detected in the paraventricular nucleus (PVN) in the same mice. C-fos IR in ORX neurons was equivalent in 8W (S, 29.4%; LE, 35.2%; HE, 35.1% ) and 12W (S, 32.0%; LE, 33.6%; HE, 36.7%) in controls, but not in db/db mice; 8W(S, 16.0%; LE, 36.4%; HE, 32.1% ) and 12W (S, 12.7%; LE, 34.0%; HE, 21.7%). The number of c-fos-positive neurons in the PVN was remarkably increased in 12W- and 8W-HE (8W-HE, 33.0; 12W-HE, 50.5) groups compared to other groups. These findings suggest that HE is not beneficial but deleterious and stressful especially for the older db/db mice with advanced diabetic pathophysiology, in which ORX-mediated defense mechanisms are insufficient.	P2-2-146 前脳基底部刺激および感覚刺激はアストロサイトCa2+シグナルとは独立に脳血流変化を起こす Cerebral blood flow modulation by basal forebrain or whisker stimulation occurs independent of astrocytic Ca2+ signaling ○高田則雄1,2, 永井てるみ1, 小澤克也1, 御子柴克彦1,3, 平瀬肇1,3 ○Norio Takata1,2, Terumi Nagai1, Katsuya Ozawa1, Katsuhiko Mikoshiba1,3, Hajime Hirase1,3 理研・BSI1, 慶應大・医・ 精神神経2, 科学技術振興機構3 RIKEN-BSI, Wako1, Dept. Neuropsychiatry, Keio Univ, Tokyo2, JST, ICORP and SORST, Kawaguchi3 Prolonged activation of the nucleus basalis of Meynert (NBM), the primary source of cholinergic projection to the cerebral cortex has been reported to cause significant increases in cerebral cortical blood flow (CBF) in rodents. While the NBM also gives rise to GABAergic and glutamatergic projections to the cerebral cortex, the NBM-driven increase of CBF has been described to be dependent in part on muscarinic acetylcholine receptors. Lately, several groups reported that astrocytes modulate local CBF via intracellular Ca2+ signaling. Considering that cortical astrocytes express mAChRs and in vivo activation of the NBM leads to mAChR-dependent Ca2+ surges in astrocytes, cholinergic modulation of CBF via astrocytic Ca2+ surges is conceivable. We report here that a single train stimulation of the NBM (stNBM; 100 Hz, 0.5 s, 200 μA) induces a biphasic (a rapid increase, followed by an overshooting slower decrease that goes back to baseline within a minute) laser Doppler flowmetry (LDF) response in the somatosensory cortex. Moreover, the stNBM-induced LDF response was sensitive to the mAChR antagonist atropine. StNBM with a weaker stimulation intensity (50 μA) induces a transient decrease. Surprisingly, we find that IP3R2 knockout mice, which lack cytosolic Ca2+ surges in astrocytes, show similar LDF responses to stNBM. We are currently dissecting the mechanism of these LDF responses by in vivo two-photon imaging and optogenetics.
P2-2-147 パルブアルブミン発現皮質神経細胞に対する興奮性・抑制性入力様式を運動野にて定量的に解析する Excitatory and Inhibitory Inputs to Parvalbumin-Expressing Interneurons in the Mouse Primary Motor Cortex ○日置寛之1, 孫在隣1, 倉本恵梨子1, 岡本慎一郎1, 王濤1, 亀田浩司2, 藤山文乃3,4, 金子武嗣1 ○Hiroyuki Hioki1, Jaerin Sohn1, Eriko Kuramoto1, Shinichiro Okamoto1, Tao Wang1, Hiroshi Kameda2, Fumino Fujiyama3,4, Takeshi Kaneko1 京都大学大学院 医学研究科 高次脳形態学1, 帝京大学医学部生理学講座2, 同志社大学大学院 脳科学研究科 神経回路形態部門3, 独立行政法人科学技術振興機構, CREST4 Dept Morphol Brain Sci, Grad Sch of Med, Kyoto Univ, Kyoto1, Dept Physio, Teikyo Univ Sch of Med, Tokyo2, Laboratory of Neural Circuitry, Doshisha University, Kyoto3, JST, CREST4 Neocortical GABAergic interneurons are divided into at least three distinct subgroups by chemical markers: 1) parvalbumin (PV)-expressing cells; 2) somatostatin (SOM)-producing cells; 3) the cells immunoreactive for other markers such as vasoactive intestinal polypeptide (VIP). PV neurons are a major component of cortical GABAergic interneurons, and play a key role in higher-order brain functions. In the previous study, we generated BAC transgenic mice expressing somatodendritic membrane-targeted GFP specifically in PV neurons, and succeeded in visualizing the dendrites and cell bodies completely. Using the transgenic mice, we revealed that PV neurons receive inhibitory inputs on the proximal portions and excitatory inputs on the distal dendrites in the S1. We further demonstrated the compartmental organization of inhibitory inputs to PV neurons. The dendritic compartment principally received inhibitory inputs from PV neurons, and the somatic compartment from VIP neurons. In the present study, we investigate the excitatory and inhibitory inputs to PV neurons in the M1, and consider the general rule of the synaptic inputs to PV neurons in the neocortex.	P2-2-148 連続経頭蓋磁気刺激によるヒト脳活動の大域的制御 Global control of human brain networks by repetitive TMS ○中川佑美1,2, 花川隆1,3,4, 水野佑治1,5, 北城圭一1,2,4,5 ○Yumi Nakagawa1,2, Takashi Hanakawa1,3,4, Yuji Mizuno1,5, Keiichi Kitajo1,2,4,5 理研BTCC1, 理研BSI 脳信号処理研究チーム2, 国立精神・神経医療研究センター3, JST さきがけ4, 東京農工大5 RIKEN BTCC, Wako, Saitama, JAPAN1, Lab. for Advanced Brain Signal Processing, RIKEN BSI, Wako, Saitama, JAPAN2, NCNP, Tokyo, JAPAN3, JST PRESTO, Kawaguchi, Saitama, JAPAN4, TUAT, Tokyo, JAPAN5 It has been suggested that synchronization of neural activity is important in mediating functional neural information processing in the human brain. To our knowledge, however, there is no study which demonstrated causal links between large-scale neural synchrony networks and brain functions in humans. Here we propose a novel approach to manipulate large-scale synchrony networks to show causal links between neural synchrony and brain functions by TMS (Transcranial magnetic stimulation)-EEG.In the current study, we use repetitive transcranial magnetic stimulation (rTMS), and we target rTMS to the visual cortex (occipital pole, 90% phosphene threshold) or the left motor cortex (90% motor threshold). We recorded single-shot TMS and repetitive 5 shots (3 different stimulus frequency) TMS-modulated ongoing brain activities while normal participants sitting on a chair with their eyes open (30 trials) fixating a cross on a display. We analyzed resting state 63ch EEG(Brainamp MR+) records (sampling rate =5000Hz, offline resampled at 1000Hz).We extracted instantaneous phase and amplitude of EEG records. Next we analyzed phase locking between EEG signals and TMS shots. We also analyzed changes in amplitude during rTMS. We found frequency-specific phase locking between rTMS and EEG signals at two different conditions (Motor area TMS and Visual area TMS). The phase locking propagated from the stimulated areas to distant brain areas prominently at the rTMS frequency. We also observed global propagation of TMS-induced amplitude changes in a frequency-specific way. The results suggest the possibility of controlling global frequency-specific synchronization networks using rTMS. We propose that we can show causal links between neural synchrony and brain functions using this novel manipulative approach.

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