一般口演
知覚 / 報酬と罰の学習 / 情動
Perception / Appetitive and Aversive Learning / Emotion
座長：佐藤 真（大阪大学大学院） |
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| 2022年7月2日 14:00～14:15 沖縄コンベンションセンター 会議場B2 第5会場
3O05a1-01
ヒト脳進化により大脳新皮質の感覚処理にかかる時間は延長した：霊長類４種における無侵襲の聴覚誘発電位計測による検討
Human brain evolution accompanied a prologation of cerebral cortical sensory processing time: a non-invasive auditory evoked potential study in four primate species
*伊藤 浩介(1)、鴻池 菜保(2)、 禰占 雅史(2)、岩沖 晴彦(2)、五十嵐 博中(1)、平田 聡(3)、中村 克樹(2)
1. 新潟大学脳研究所、2. 京都大学霊長類研究所、3. 京都大学野生動物研究センター
*Kosuke Itoh(1), Naho Konoike(2), Masafumi Nejime(2), Haruhiko Iwaoki(2), Hironaka Igarashi(1), Satoshi Hirata(3), Katsuki Nakamura(2)
1. Brain Research Institute, Niigata University, 2. Primate Research Institute, Kyoto University, 3. Wildlife Research Center, Kyoto University
Keyword: auditory cortex, evolution, nonhuman primate, auditory evoked potentials
“Bigger is better” is a simple and widely accepted principle in brain evolution. An important assumption behind this hypothesis is that a larger brain contains a greater number of neurons, particularly cortical neurons, which augments the capacity for complex information processing. However, there is a sometimes overlooked disadvantage to having an increased number of cortical neurons, namely, a prolonged neural-processing time. The evolution of human cognition is expected to have accompanied a prolongation of net neural-processing time due to the accumulation of processing time of individual neurons over an increased number of neurons.
Here, we confirmed this prediction and quantified the amount of prolongation in vivo, using noninvasive measurements of brain responses to sounds in unanesthetized human and nonhuman primates. Latencies of the N1 component of auditory-evoked potentials recorded from the scalp were approximately 40, 50, 60, and 100 ms for the common marmoset (n = 4), rhesus monkey (n = 7), chimpanzee (n = 1), and human (n = 18), respectively. Importantly, the prominent increase in human N1 latency could not be explained by the physical lengthening of the auditory pathway, and therefore reflected an extended dwell time for auditory cortical processing.
An elongation of the auditory cortical processing time entails both merits and demerits. Slow processing is disadvantageous in situations where fast identifications of sounds are required, such as when detecting the sound of a predator. On the other hand, a widened processing time has the advantage of allowing the auditory input to be integrated over a longer time window, which is beneficial for analyzing the time-varying temporal structures of sounds, such as those important for the segmentation and categorization of phonemes. A novel hypothesis concerning human brain evolution then emerges: the increase in cortical neuronal number widened the timescale of sensory cortical processing, the benefits of which outweighed the disadvantage of slow cognition and reaction. | | 2022年7月2日 14:15～14:30 沖縄コンベンションセンター 会議場B2 第5会場
3O05a1-02
情報表現を共有する脳内ワークスペース
A neural workspace for representation sharing
*可部 泰生(1)、笹井 俊太朗(2)
1. 東京大学大学院情報理工学系研究科、2. 株式会社アラヤ
*Yasuo Kabe(1), Shuntaro Sasai(2)
1. Grad Sch Inf Sci & Tech, Univ of Tokyo, Tokyo, Japan, 2. Araya, Inc., Tokyo, Japan
Keyword: ABSTRACTION, GLOBAL WORKSPACE, SHARED RESPONSE MODEL, NATURALISTIC STIMULI
The human brain can transform primary sensory inputs into general concepts which allow for complex cognition. This process of abstraction is the hallmark of human intelligence, which separates them from other animals or intelligent machines. Confronted with the task of handling information from multiple regions specialized in different functions, the brain performs abstraction to extract modality-agnostic concepts. For instance, while you're watching a movie, the auditory and visual stimuli are constantly being grounded to the object being portrayed. Although this process of abstraction is crucial in deepening our understanding of human intelligence, how information is being abstracted while propagating in the brain is yet to be known.
Here we show that the fronto-parietal region including DLPFC play a key role in governing information transfer from auditory and visual regions. We identified the region as a hub for communicating abstract concepts by extracting fMRI activity in a naturalistic movie-watching scenario and applying the shared response model (SRM). The SRM was used to quantify the information sharing between regions of interests (ROIs) given by a coarse-grained version of the Glasser parcellation and compared against results given by functional connectivity. Furthermore, the representation of abstract concepts became robust and shared its semantic structure as it gets closer to the region as shown by attempting decoding of depicted animal type. The decoding of animal type was controlled against decoding of low-level audio and visual confounds. This result suggests the fronto-parietal region functions as the hub at which abstract concepts are represented given the situation at hand.
Further looking into the process of abstraction from neural activity during cognitive tasks is promising in unveiling how the abstracted concepts are manipulated in the brain. This should yield insights not only in understanding human intelligence but also in developing artificial general intelligence. | | 2022年7月2日 14:30～14:45 沖縄コンベンションセンター 会議場B2 第5会場
3O05a1-03
回避記憶の形成と大脳皮質のArcの活性化にはドーパミンD1受容体を介した神経伝達が必要である
Neurotransmission through dopamine D1 receptor is required for aversive memory formation and Arc activation in the cerebral cortex
*笹岡 俊邦(1)、齊藤 奈英(1)、田井中 一貴(1)、マクファーソン トム(2)、疋田 貴俊(2)、山口 瞬(3,4)
1. 新潟大学脳研究所、2. 大阪大学蛋白質研究所、3. 岐阜大学大学院医学系研究科、4. 岐阜大学生命の鎖統合研究センター
*Toshikuni Sasaoka(1), Nae Saito(1), Kazuki Tainaka(1), Tom Macpherson(2), Takatoshi Hikida(2), Shun Yamaguchi(3,4)
1. Brain Research Institute, Niigata University, Niigata, Japan, 2. Institute for Protein Research, Osaka University, Osaka, Japan, 3. raduate School of Medicine, Gifu University, Gifu, Japan, 4. Center for Highly Advanced Integration of Nano and Life Sciences, Gifu University, Gifu, Japan
Keyword: dopamine D1 receptor, aversive memory, Arc, Arg3.1, three-dimensional imaging
Dopaminergic neurotransmission is considered to play an important role not only in reward-based learning, but also in aversive learning. Here, we investigated the role of dopaminergic neurotransmission via dopamine D1 receptors (D1Rs) in aversive memory formation in a passive avoidance (PA) test using D1R knockdown (KD) mice, in which the expression of D1Rs can conditionally and reversibly be controlled by doxycycline (Dox) treatment (+) (Chiken et al., 2015). To elucidate neural activity in discrete brain regions, indicated by expression of the immediate early gene, Arc, during aversive learning, we crossed D1RKD mice with Arc-dVenus mice. We found that suppression of D1R expression during memory formation in D1RKD Dox (+) mice resulted in markedly lower performance in the PA test than in D1RKD Dox non-treatment (-) or WT mice. When D1R expression was recovered in these D1RKD Dox (+) mice, their performance became comparable to that of D1RKD Dox (-) mice. These results suggested that D1R deficiency was responsible for impaired aversive memory formation. D1Rs are known to play an important role in the regulation of both hippocampus-dependent plasticity and hippocampus-dependent memory, and are pivotal in conferring the properties of novelty and reward to information being processed by the hippocampus. D1Rs in the cerebral cortex have been implicated in memory-induced long-term plasticity and memory formation and are suggested to control the storage of long-term aversive memories. Given the important roles of D1Rs in these regions in learning and memory, we investigated the expression levels of Arc, known to be located downstream of D1R-mediated neural transmission and suppressed by D1R inactivation, in the hippocampus and cerebral cortex during learning and of an aversive memory. Interestingly, we did not observe any differences between D1RKD Dox (+) and D1RKD Dox (-) groups in CA1 and CA2 Arc expression. However, D1R-suppressed mice exhibited lower expression of Arc in the cortex, including layers 1-3 and 5–6 of the cerebral cortex (including the somatosensory and motor cortices and excluding the visual cortex), and layers 5–6 of the visual cortex compared with D1R-expressing mice, indicating that D1R inhibition led to suppressed Arc expression. As we controlled for the confounding effects of visual stimuli (by performing the experiment in a dark room), these observed patterns could be attributed to the electric footshock. | | 2022年7月2日 14:45～15:00 沖縄コンベンションセンター 会議場B2 第5会場
3O05a1-04
慢性社会ストレスはシナプスの中央代謝系を変化して抑うつを誘導する
Chronic social stress alters synaptic central metabolism for depression
*永井 裕崇(1)、永井 碧(1)、沼 知里(1)、山下 朋美(2)、川島 祐介(3)、大野 伸彦(4,5)、片岡 洋祐(6,7)、新間 秀一(8,9)、清末 優子(7)、加藤 太朗(2)、曽我 朋義(10)、古屋敷 智之(1)
1. 神戸大学大学院医学研究科、2. 大日本住友製薬株式会社、3. かずさDNA研究所、4. 自治医科大学医学部、5. 生理学研究所、6. 理研―JEOL連携センター、7. 理研生命機能科学研究センター、8. 大阪大学大学院工学研究科、9. 大阪大学・島津分析イノベーション協働研究所、10. 慶應義塾大学先端生命科学研究所
*Hirotaka Nagai(1), Midori Nagai(1), Chisato Numa(1), Tomomi Yamashita(2), Yusuke Kawashima(3), Nobuhiko Ohno(4,5), Yosky Kataoka(6,7), Shuichi Shimma(8,9), Yuko Mimori-Kiyosue(7), Taro Kato(2), Tomoyoshi Soga(10), Tomoyuki Furuyashiki(1)
1. Grad Sch Med, Kobe Univ, Kobe, Japan, 2. Sumitomo Dainippon Pharma, Osaka, Japan, 3. Kazusa DNA Res Inst, Kisarazu, Japan, 4. Jichi Med Univ, Shimotsuke, Japan, 5. Natl Inst Phys Sci, Okazaki, Japan, 6. RIKEN-JEOL Collaboration Center, Kobe, Japan, 7. RIKEN Center Biosystems Dynamics Res, Kobe, Japan, 8. Grad Sch Engineering, Osaka Univ, Suita, Japan, 9. Osaka Univ Shimadzu Analytical Innovation Lab, Suita, Japan, 10. Inst Adv Biosci, Keio Univ, Tsuruoka, Japan
Keyword: Social defeat stress, Medial prefrontal cortex, Multiomics analysis, Central metabolism
Excessive or chronic social stress induces emotional and cognitive disturbances and precipitates mental illness. Altered neuronal morphology and functions in the medial prefrontal cortex (mPFC) underlie these behavioral abnormalities. However, its subcellular mechanisms remain elusive. Here we examined ultrastructural and multi-omics changes in the mPFC after social stress in mice. Social stress caused the loss of dendritic branches with morphological alterations of subcellular mitochondria and induced synaptic shrinkage selectively at the synapses with mitochondria. Multi-omics and functional analyses revealed that social stress deteriorated mitochondrial functions with altered mitochondrial proteome at synapses and dysregulated central metabolic pathways in the mPFC. Pharmacological manipulation targeting mitochondria attenuated the synaptic shrinkage and depression-related behaviors. These findings demonstrate that chronic social stress alters the central metabolism at mPFC synapses, leading to neuronal pathology and depression-related behaviors. | |
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