一般口演（Oral）

Oral Sensory information Processing 一般口演感覚情報処理

7月27日（土）9:45～10:00　第10会場（万代島ビル　6F　会議室） 3O-10m2-1 音に呼応する内耳感覚上皮帯の非典型な動きとその分析 Takeru Ota（太田岳）¹，Fumiaki Nin（任書晃）¹，Samuel Choi（崔森悦）^2,3，Hiroshi Hibino（日比野浩）^1,2 ¹新潟大院医歯分子生理 ²AMED-CREST, AMED, 新潟 ³新潟大工 Hearing is essential for mammals including humans. The electrical signals necessary for excitation of auditory nerve are produced by the cochlea of the inner ear. This process is triggered by sound-evoked nanoscale vibrations in the sensory epithelium inside the cochlea. The epithelium contains outer hair cells that have mechanosensory hair bundles at the apical surface. The deflection of the bundles enters cation through ion channels. The epithelial vibrations are modulated by cation-induced elastic motions in the cell bodies. Prestin, a motor protein located in the basolateral membrane of the cells, is responsible for amplifying vibration amplitudes of the tissue. Owing to the regulation, the amplitudes increases nonlinearly with increasing the sound pressure, which is known as nonlinear compression. Nonetheless, how the vibrations are regulated in vivo has not yet been fully elucidated. Here we develop an advanced laser interferometry that precisely detects the vibrations. When a live guinea pig was exposed to acoustic stimuli, the interferometer quantitatively recorded the vibration amplitude of the sensory epithelium as described elsewhere. Additionally, an upward baseline shift of several nanometers was also detected. This motion was negligible when the animal was dead. In addition, with pharmacological perturbation of its motions by administration of sodium salicylate which is a prestin-specific inhibitor, the origin of the shift was identified as the motor function of the cell body. A theoretical approach further suggested that the shift protects the epithelium from injury induced by strong stimuli.		7月27日（土）10:00～10:15　第10会場（万代島ビル　6F　会議室） 3O-10m2-2 Revealing context-specific global cortical processing by wide-field calcium imaging and optogenetic stimulation mapping Keita Tamura（Tamura Keita），Vahid Esmaeili（Esmaeili Vahid），Sylvain Crochet（Crochet Sylvain），Carl C.H. Petersen（Petersen Carl C.H.） Carl Petersen Lab, Brain Mind Institute, EPFL, Lausanne, Switzerland To quickly switch behavior in changing environments, switching of neural computations would be an essential process. If this process is impaired, we may repeat a single action many times even when that action is no longer appropriate. However, whether and how such neural switching occurs remains unclear. Here, we visualized dynamic changes in global cortical circuits between different behavioral contexts. First, we performed optogenetic stimulation mapping of the dorsal cortex in Thy1-ChR2 mice, and localized the tongue/jaw motor area (tjM1) in which optogenetic stimulation evoked jaw-opening movements. Interestingly, stimulation of this area provoked tongue protrusion movements only in contexts where mice could lick for liquid reward. Next, we performed wide-field calcium imaging in transgenic mice expressing a red fluorescent calcium indicator (RCaMP) during a context discrimination task. In the task, mice licked for reward in response to an auditory `go' cue when a preceding whisker contextual cue predicted the availability of reward, while mice withheld licking after the `go' cue when there was no contextual cue. In correct trials, the cortical activity after the auditory `go' cue expanded to tjM1 only when the whisker contextual cue predicted the reward availability. Our observations demonstrate functional and causal switching of cortical circuits to produce context-matched behavior. Optogenetic stimulation mapping under wide-field calcium imaging in task-performing mice will further reveal the functional cortical network and its dynamic reorganization driven by behavioral demands.

7月27日（土）10:15～10:30　第10会場（万代島ビル　6F　会議室） 3O-10m2-3 表情認知における内受用感覚の役割 Tomoko Isomura（磯村朋子）^1,2，Manos Tsakiris（Tsakiris Manos）² ¹早稲田大　理工総合研究所 ²Dept Psychol, Royal Holloway University of London, Egham, United Kingdom It has been proposed that people understand and interpret other's emotional expressions by internally replicating (`simulating') the observed expression in their own bodies. While the simulation process requires people to access and analyze their own bodily states to reference representation of the associated states, it is known that people vary in the extent to which they are sensitive to the afferent signals arising from within the body. Accordingly, the ability to recognize other's emotional expression relies, at least in part, on one's sensibility to the physiological condition of the body. The sense of the physiological condition of the body is referred to as interoception, whose role in emotion recognition has recently been paid great attention. Nevertheless, it still remains unclear how the interoceptive process impacts on the recognition of facial emotions with varied intensity, from subtle to intense emotional expressions. In the present study, therefore, we tested the relationship between individual's interoceptive ability and the manner to recognize other's facial emotional expressions with varied intensity. We first collected data for interoceptive ability from 150 subjects using a heartbeat tracking task, and invited those who showed particularly high performance (n=17) and low performance (n=19) to a subsequent emotion recognition task. In the emotion recognition task, participants were asked to rate the intensity of presented faces which were morphed photos ranging in appearance from 100% neutral to 100% emotional (anger/fear/happiness) with 10% increments. The results showed that people with high interoceptive ability rated intense emotional expressions more intensely, whereas they rated subtle emotional expressions less intensely, as compared to those with low interoceptive ability. These results indicate that people with high interoceptive ability are likely to possess wider range of dimension for perception of intensity in facial emotional expressions, suggesting the role of interoception in precisely mapping the degree of intensity in the emotional signals expressed by others. We will further discuss a model describing how interoception mediates the link between physiological change of one's own body and recognition of other's emotional expressions, together with the physiological data that are currently under collection.		7月27日（土）10:30～10:45　第10会場（万代島ビル　6F　会議室） 3O-10m2-4 Spontaneous cingulate high-current spikes signal normal and pathological pain states Bai-Chuang Shyu（Shyu Bai-Chuang），Hsi-Chien Shih（Shih Hsi-Chien） Institute of Biomedical Sciences, Academia Sinica Prominent 7-12 Hz oscillations in frontal cortical networks in rats have been reported. However, the mechanism of generation and the physiological function of this brain rhythm have not yet been clarified. Multi-channel extracellular field potentials of the anterior cingulate cortex (ACC) were recorded and analyzed using the current source density method in halothane-anesthetized rats. Spontaneous high-current spikes (HCSs) were localized in the deep part of layer II/III and upper part of layer V of the ACC. The frequency of HCSs in the ACC was 7-12 Hz, with an amplitude of 6.5 ± 0.76 mV/mm2 and duration of 55.24 ± 2.43 ms. The power density significantly decreased (84.56% ± 6.93%, p < 0.05, t-test) after pinching the hindpaw and significantly increased (149.28% ± 15.96%) after treatment with morphine. The suppressive effect of pinching was reversed by naloxone (0.7 mg/kg, i.p.). HCSs coincided with initiation of the depolarization of cingulate neurons and remained in a depolarized upstate. The occurrence of cingulate HCSs was persistently preceded by a hyperpolarization phase and a burst of multiunit spike activity in the medial dorsal thalamic nucleus (MD). Spontaneous field-potential oscillations changed from 10 Hz to a lower band (i.e., ~7.5 Hz) when a central poststroke pain (CPSP) condition was induced. The CPSP group had a higher average coherence coefficient compared with the control group. Our results indicate that spontaneous cingulate cortical HCSs could be initiated by thalamocortical synaptic inputs from the MD and maintained by intracortical neuronal upstate mechanisms in physiological and pathological pain states.