Updated on 2024/09/02

写真a

 
MUKAI Yasutaka
 
Organization
Graduate School of Science Assistant Professor
Graduate School
Graduate School of Science
Undergraduate School
School of Science Department of Biological Science
Title
Assistant Professor
External link

Degree 3

  1. Doctor (Medicine) ( 2021.3   Nagoya University ) 

  2. Master (Medical Science) ( 2017.3   Nagoya University ) 

  3. Bachelor (Science) ( 2015.3   Nagoya University ) 

Research Areas 5

  1. Life Science / Pharmacology

  2. Life Science / Molecular biology

  3. Life Science / Physiology

  4. Life Science / Neuroscience-general

  5. Life Science / Function of nervous system

Research History 4

  1. Nagoya University   Graduate School of Science   Assistant Professor

    2024.9

  2. Nagoya City University   Graduate School of Pharmaceutical Sciences Department of Neuropharmacology

    2024.4 - 2024.8

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  3. Hokkaido University   Department of Cellular Pharmacology, Graduate School of Medicine

    2023.4 - 2024.3

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    Country:Japan

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  4. Nagoya University   Research Institute of Environmental Medicine

    2015.4 - 2023.3

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Education 3

  1. Nagoya University   Graduate School of Medicine   Doctoral Course in Integrated Medicine

    2017.4 - 2021.3

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  2. Nagoya University   Graduate School of Medicine   Master Course in Medical Science

    2015.4 - 2017.3

  3. Nagoya University   School of Science   Department of Biological Science

    2011.4 - 2015.3

Professional Memberships 2

  1. The Physiological Society of Japan

    2016.11

  2. The Japan Neuroscience Society

    2016.1

Awards 1

  1. AND 2023 Poster award

    2023.9   Association for the study of neurons and diseases   Identification of substances that modulate the activity of noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai

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Papers 10

  1. Prostaglandin E<sub>2</sub>Induces Long-Lasting Inhibition of Noradrenergic Neurons in the Locus Coeruleus and Moderates the Behavioral Response to Stressors Reviewed

    Yasutaka Mukai, Tatsuo S. Okubo, Michael Lazarus, Daisuke Ono, Kenji F. Tanaka, Akihiro Yamanaka

    The Journal of Neuroscience   Vol. 43 ( 47 ) page: 7982 - 7999   2023.11

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    Authorship:Lead author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Society for Neuroscience  

    Neuronal activity is modulated not only by inputs from other neurons but also by various factors, such as bioactive substances. Noradrenergic (NA) neurons in the locus coeruleus (LC-NA neurons) are involved in diverse physiological functions, including sleep/wakefulness and stress responses. Previous studies have identified various substances and receptors that modulate LC-NA neuronal activity through techniques including electrophysiology, calcium imaging, and single-cell RNA sequencing. However, many substances with unknown physiological significance have been overlooked. Here, we established an efficient screening method for identifying substances that modulate LC-NA neuronal activity through intracellular calcium ([Ca<sup>2+</sup>]<sub>i</sub>) imaging using brain slices. Using both sexes of mice, we screened 53 bioactive substances, and identified five novel substances: gastrin-releasing peptide, neuromedin U, and angiotensin II, which increase [Ca<sup>2+</sup>]<sub>i</sub>, and pancreatic polypeptide and prostaglandin D<sub>2</sub>, which decrease [Ca<sup>2+</sup>]<sub>i</sub>. Among them, neuromedin U induced the greatest response in female mice. In terms of the duration of [Ca<sup>2+</sup>]<sub>i</sub>change, we focused on prostaglandin E<sub>2</sub>(PGE<sub>2</sub>), since it induces a long-lasting decrease in [Ca<sup>2+</sup>]<sub>i</sub>via the EP<sub>3</sub>receptor. Conditional knock-out of the receptor in LC-NA neurons resulted in increased depression-like behavior, prolonged wakefulness in the dark period, and increased [Ca<sup>2+</sup>]<sub>i</sub>after stress exposure. Our results demonstrate the effectiveness of our screening method for identifying substances that modulate a specific neuronal population in an unbiased manner and suggest that stress-induced prostaglandin E<sub>2</sub>can suppress LC-NA neuronal activity to moderate the behavioral response to stressors. Our screening method will contribute to uncovering previously unknown physiological functions of uncharacterized bioactive substances in specific neuronal populations.

    SIGNIFICANCE STATEMENTBioactive substances modulate the activity of specific neuronal populations. However, since only a limited number of substances with predicted effects have been investigated, many substances that may modulate neuronal activity have gone unrecognized. Here, we established an unbiased method for identifying modulatory substances by measuring the intracellular calcium signal, which reflects neuronal activity. We examined noradrenergic (NA) neurons in the locus coeruleus (LC-NA neurons), which are involved in diverse physiological functions. We identified five novel substances that modulate LC-NA neuronal activity. We also found that stress-induced prostaglandin E<sub>2</sub>(PGE<sub>2</sub>) may suppress LC-NA neuronal activity and influence behavioral outcomes. Our screening method will help uncover previously overlooked functions of bioactive substances and provide insight into unrecognized roles of specific neuronal populations.

    DOI: 10.1523/jneurosci.0353-23.2023

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  2. Functional roles of REM sleep Reviewed

    Yasutaka Mukai, Akihiro Yamanaka

    Neuroscience Research   Vol. 189   page: 44 - 53   2023.4

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    Authorship:Lead author   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.neures.2022.12.009

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  3. Cre-dependent ACR2-expressing reporter mouse strain for efficient long-lasting inhibition of neuronal activity Reviewed

    Yasutaka Mukai, Yan Li, Akiyo Nakamura, Noriaki Fukatsu, Daisuke Iijima, Manabu Abe, Kenji Sakimura, Keiichi Itoi, Akihiro Yamanaka

    Scientific Reports   Vol. 13 ( 1 )   2023.3

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    Optogenetics is a powerful tool for manipulating neuronal activity by light illumination with high temporal and spatial resolution. Anion-channelrhodopsins (ACRs) are light-gated anion channels that allow researchers to efficiently inhibit neuronal activity. A blue light-sensitive ACR2 has recently been used in several in vivo studies; however, the reporter mouse strain expressing ACR2 has not yet been reported. Here, we generated a new reporter mouse strain, LSL-ACR2, in which ACR2 is expressed under the control of Cre recombinase. We crossed this strain with a noradrenergic neuron-specific driver mouse (NAT-Cre) to generate NAT-ACR2 mice. We confirmed Cre-dependent expression and function of ACR2 in the targeted neurons by immunohistochemistry and electrophysiological recordings in vitro, and confirmed physiological function using an in vivo behavioral experiment. Our results show that the LSL-ACR2 mouse strain can be applied for optogenetic inhibition of targeted neurons, particularly for long-lasting continuous inhibition, upon crossing with Cre-driver mouse strains. The LSL-ACR2 strain can be used to prepare transgenic mice with homogenous expression of ACR2 in targeted neurons with a high penetration ratio, good reproducibility, and no tissue invasion.

    DOI: 10.1038/s41598-023-30907-2

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    Other Link: https://www.nature.com/articles/s41598-023-30907-2

  4. Glutamatergic signaling from melanin-concentrating hormone-producing neurons: A requirement for memory regulation, but not for metabolism control Reviewed

    Xuan Thang Pham, Yoshifumi Abe, Yasutaka Mukai, Daisuke Ono, Kenji F Tanaka, Yu Ohmura, Hiroaki Wake, Akihiro Yamanaka

    PNAS Nexus   Vol. 3 ( 7 )   2024.6

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    Publishing type:Research paper (scientific journal)   Publisher:Oxford University Press (OUP)  

    Abstract

    Melanin-concentrating hormone-producing neurons (MCH neurons), found mainly in the lateral hypothalamus and surrounding areas, play essential roles in various brain functions, including sleep and wakefulness, reward, metabolism, learning, and memory. These neurons coexpress several neurotransmitters and act as glutamatergic neurons. The contribution of glutamate from MCH neurons to memory- and metabolism-related functions has not been fully investigated. In a mouse model, we conditionally knocked out Slc17a6 gene, which encodes for vesicular glutamate transporter 2 (vGlut2), in the MCH neurons exclusively by using two different methods: the Cre recombinase/loxP system and in vivo genome editing using CRISPR/Cas9. Then, we evaluated several aspects of memory and measured metabolic rates using indirect calorimetry. We found that mice with MCH neuron-exclusive vGlut2 ablation had higher discrimination ratios between novel and familiar stimuli for novel object recognition, object location, and three-chamber tests. In contrast, there was no significant change in body weight, food intake, oxygen consumption, respiratory quotient, or locomotor activity. These findings suggest that glutamatergic signaling from MCH neurons is required to regulate memory, but its role in regulating metabolic rate is negligible.

    DOI: 10.1093/pnasnexus/pgae275

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    Other Link: https://academic.oup.com/pnasnexus/article-pdf/3/7/pgae275/58598945/pgae275.pdf

  5. Chronic pain enhances excitability of corticotropin-releasing factor-expressing neurons in the oval part of the bed nucleus of the stria terminalis Reviewed

    Ryoko Uchida, Yasutaka Mukai, Taiju Amano, Kenji Sakimura, Keiichi Itoi, Akihiro Yamanaka, Masabumi Minami

    Molecular Brain   Vol. 17 ( 1 )   2024.5

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    Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    Abstract

    We previously reported that enhanced corticotropin-releasing factor (CRF) signaling in the bed nucleus of the stria terminalis (BNST) caused the aversive responses during acute pain and suppressed the brain reward system during chronic pain. However, it remains to be examined whether chronic pain alters the excitability of CRF neurons in the BNST. In this study we investigated the chronic pain-induced changes in excitability of CRF-expressing neurons in the oval part of the BNST (ovBNST<sup>CRF</sup> neurons) by whole-cell patch-clamp electrophysiology. CRF-Cre; Ai14 mice were used to visualize CRF neurons by tdTomato. Electrophysiological recordings from brain slices prepared from a mouse model of neuropathic pain revealed that rheobase and firing threshold were significantly decreased in the chronic pain group compared with the sham-operated control group. Firing rate of the chronic pain group was higher than that of the control group. These data indicate that chronic pain elevated neuronal excitability of ovBNST<sup>CRF</sup> neurons.

    DOI: 10.1186/s13041-024-01094-6

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    Other Link: https://link.springer.com/article/10.1186/s13041-024-01094-6/fulltext.html

  6. Deficiency of orexin signaling during sleep is involved in abnormal REM sleep architecture in narcolepsy Reviewed

    Hiroto Ito, Noriaki Fukatsu, Sheikh Mizanur Rahaman, Yasutaka Mukai, Shuntaro Izawa, Daisuke Ono, Thomas S. Kilduff, Akihiro Yamanaka

    Proceedings of the National Academy of Sciences   Vol. 120 ( 41 )   2023.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Proceedings of the National Academy of Sciences  

    Narcolepsy is a sleep disorder caused by deficiency of orexin signaling. However, the neural mechanisms by which deficient orexin signaling causes the abnormal rapid eye movement (REM) sleep characteristics of narcolepsy, such as cataplexy and frequent transitions to REM states, are not fully understood. Here, we determined the activity dynamics of orexin neurons during sleep that suppress the abnormal REM sleep architecture of narcolepsy. Orexin neurons were highly active during wakefulness, showed intermittent synchronous activity during non-REM (NREM) sleep, were quiescent prior to the transition from NREM to REM sleep, and a small subpopulation of these cells was active during REM sleep. Orexin neurons that lacked orexin peptides were less active during REM sleep and were mostly silent during cataplexy. Optogenetic inhibition of orexin neurons established that the activity dynamics of these cells during NREM sleep regulate NREM–REM sleep transitions. Inhibition of orexin neurons during REM sleep increased subsequent REM sleep in “orexin intact” mice and subsequent cataplexy in mice lacking orexin peptides, indicating that the activity of a subpopulation of orexin neurons during the preceding REM sleep suppresses subsequent REM sleep and cataplexy. Thus, these results identify how deficient orexin signaling during sleep results in the abnormal REM sleep architecture characteristic of narcolepsy.

    DOI: 10.1073/pnas.2301951120

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  7. Neural mechanisms underlying uninstructed orofacial movements during reward-based learning behaviors Reviewed

    Wan-Ru Li, Takashi Nakano, Kohta Mizutani, Takanori Matsubara, Masahiro Kawatani, Yasutaka Mukai, Teruko Danjo, Hikaru Ito, Hidenori Aizawa, Akihiro Yamanaka, Carl C.H. Petersen, Junichiro Yoshimoto, Takayuki Yamashita

    Current Biology   Vol. 33 ( 16 ) page: 3436 - 3451.e7   2023.8

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.cub.2023.07.013

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  8. Primary motor cortex drives expressive facial movements related to reward processing in mice

    Wanru Li, Takashi Nakano, Kohta Mizutani, Masahiro Kawatani, Takanori Matsubara, Teruko Danjo, Yasutaka Mukai, Akihiro Yamanaka, Hikaru Ito, Hidenori Aizawa, Carl C. H. Petersen, Junichiro Yoshimoto, Takayuki Yamashita

        2022.10

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    Publisher:Cold Spring Harbor Laboratory  

    ABSTRACT

    Animals exhibit expressive facial movements in a wide range of behavioral contexts. However, the underlying neural mechanisms remain enigmatic. In reward-based learning tasks, mice make expressive movements with their whiskers and nose at the timings of reward expectation and acquisition. Here we show that optogenetic stimulation of midbrain dopamine neurons (oDAS) as a reward is sufficient to induce such expressive movements. Pavlovian conditioning with a sensory cue and oDAS elicited both cue-locked (reward-expecting) and oDAS-aligned (reward-acquiring) orofacial movements. Inhibition or knock-out of dopamine D1 receptors in the nucleus accumbens inhibited oDAS-induced motion but spared cue-locked motion. Silencing the whisker primary motor cortex (wM1) abolished both oDAS-induced and cue-locked orofacial movements. We found specific neuronal populations in wM1 representing either oDAS-aligned or cue-locked whisker movements. Thus, reward-acquiring and reward-expecting facial movements are driven by accumbal D1 receptor-dependent and -independent neuronal mechanisms, respectively, both dominantly regulated by wM1 activity.

    DOI: 10.1101/2022.10.28.514159

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  9. Functional Interaction Between GABAergic Neurons in the Ventral Tegmental Area and Serotonergic Neurons in the Dorsal Raphe Nucleus Reviewed International journal

    Sheikh Mizanur Rahaman, Srikanta Chowdhury, Yasutaka Mukai, Daisuke Ono, Hiroshi Yamaguchi, Akihiro Yamanaka

    Frontiers in Neuroscience   Vol. 16   page: 877054 - 877054   2022.5

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Frontiers Media SA  

    GABAergic neurons in the ventral tegmental area (VTA) have brain-wide projections and are involved in multiple behavioral and physiological functions. Here, we revealed the responsiveness of Gad67+ neurons in VTA (VTA<sub>Gad67+</sub>) to various neurotransmitters involved in the regulation of sleep/wakefulness by slice patch clamp recording. Among the substances tested, a cholinergic agonist activated, but serotonin, dopamine and histamine inhibited these neurons. Dense VTA<sub>Gad67+</sub> neuronal projections were observed in brain areas regulating sleep/wakefulness, including the central amygdala (CeA), dorsal raphe nucleus (DRN), and locus coeruleus (LC). Using a combination of electrophysiology and optogenetic studies, we showed that VTA<sub>Gad67+</sub> neurons inhibited all neurons recorded in the DRN, but did not inhibit randomly recorded neurons in the CeA and LC. Further examination revealed that the serotonergic neurons in the DRN (DRN<sub>5–HT</sub>) were monosynaptically innervated and inhibited by VTA<sub>Gad67+</sub> neurons. All recorded DRN<sub>5–HT</sub> neurons received inhibitory input from VTA<sub>Gad67+</sub> neurons, while only one quarter of them received inhibitory input from local GABAergic neurons. Gad67+ neurons in the DRN (DRN<sub>Gad67+</sub>) also received monosynaptic inhibitory input from VTA<sub>Gad67+</sub> neurons. Taken together, we found that VTA<sub>Gad67+</sub> neurons were integrated in many inputs, and their output inhibits DRN<sub>5–HT</sub> neurons, which may regulate physiological functions including sleep/wakefulness.

    DOI: 10.3389/fnins.2022.877054

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  10. The oxytocin system regulates tearing

    Shigeru Nakamura, Toshihiro Imada, Kai Jin, Michiko Shibuya, Hisayo Sakaguchi, Fumiya Izumiseki, Kenji F Tanaka, Masaru Mimura, Kastuhiro Nishimori, Natsumi Kambara, Nozomi Hirayama, Itsuka Kamimura, Kensaku Nomoto, Kazutaka Mogi, Takefumi Kikusui, Yasutaka Mukai, Akihiro Yamanaka, Kazuo Tsubota

        2022.3

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    Publisher:Cold Spring Harbor Laboratory  

    Abstract

    Tears are an exocrine physiological fluid secreted onto the ocular surface from the lacrimal apparatus in all mammals. Limited research has been conducted on the functional neuronal circuitry of tear production. In particular, the neuronal mechanisms of emotional tearing, which is a physiological reaction harmonized with enhanced emotional arousal and assumed to be unique to humans, remain unclear. We identified that the oxytocin neurons in the paraventricular hypothalamus is functionally projected to the oxytocin receptor-expressing neurons in the lacrimation center of the superior salivatory nucleus. Optogenetic activation or inhibition of these neurons and/or receptors can modulate the superior salivatory nucleus dependent tear secretion mediated through oxytocin. Moreover, we identified that maternal behavior, nociceptive behavior stimulation, and aversive memory retrieval are linked to tearing in mice, and that these emotional linked tearing are suppressed by optogenetic inhibition of the corresponding oxytocin system. Thus, tearing could be regulated through functional connections between central oxytocin systems in the paraventricular hypothalamus and the superior salivatory nucleus.

    DOI: 10.1101/2022.03.08.483433

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Books 1

  1. 精神医学領域の論文を読みこなすキーワード100!

    向井康敬, 山中章弘( Role: Contributor ,  23. 視床下部)

    新興医学出版社  2022.12  ( ISBN:9784880028866

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Presentations 11

  1. Identification of substances that modulate the activity of noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai, Michael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    Association for Study of Neurons and Diseases, The 16th International Conference for Neurons and Brain Disease  2023.9.20 

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    Event date: 2023.9

    Language:English   Presentation type:Poster presentation  

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  2. Physiological function of prostaglandin E2-induced sustained suppression of activity of noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai, Michael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    Neuro2022  2022.7.1 

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    Event date: 2022.6 - 2022.7

    Language:Japanese   Presentation type:Oral presentation (general)  

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  3. Physiological function of prostaglandin E2-induced long lasting inhibition of noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai, Michael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    2022.3.18 

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    Event date: 2022.3

    Language:English   Presentation type:Poster presentation  

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  4. 特定神経の活動を調節する物質のスクリーニングと、それを用いた生理機能の解明 Invited

    向井康敬, 永山綾子, 井樋慶一, 山中章弘

    日本睡眠学会 第46回定期学術集会  2021.9.23 

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    Event date: 2021.9

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

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  5. Searching for physiological functions of prostaglandin E2 in noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai, Michael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    2021.7.28 

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    Event date: 2021.7

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  6. Long-lasting regulatory mechanism of noradrenergic neurons in the locus coeruleus by prostaglandin E2 Invited

    Yasutaka Mukai

    2021.6.11 

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    Event date: 2021.6

    Language:Japanese   Presentation type:Oral presentation (general)  

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  7. Prostaglandin E2 induces long-lasting calcium decrease of noradrenergic neurons in the locus coeruleus via EP3 receptor

    Yasutaka Mukai, MIchael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    The 98th Annual Meeting of The Physiological Society of Japan  2021.3.28 

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    Event date: 2021.3

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  8. Identification of factors regulating activity of corticotropin-releasing factor-producing neurons in the paraventricular nucleus of the hypothalamus International conference

    Yasutaka Mukai, Ayako Nagayama, Keiichi Itoi, Akihiro Yamanaka

    SfN Global Connectome  2021.1.12 

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    Event date: 2021.1

    Language:English   Presentation type:Poster presentation  

    Country:United States  

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  9. Identification of substances that modulate the activity of noradrenergic neurons in the locus coeruleus

    Yasutaka Mukai, Michael Lazarus, Takeharu Nagai, Kenji F Tanaka, Akihiro Yamanaka

    The 46th Annual Meeting of the Japan Neuroscience Society  2023.8.3 

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  10. Prostaglandin E2 induces sustained suppression of noradrenergic neurons in the locus coeruleus to moderate stress response

    Yasutaka Mukai, Tatsuo S. Okubo, Michael Lazarus, Daisuke Ono, Kenji F. Tanaka, Akihiro Yamanaka

    2024.3.29 

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  11. Neuromodulator dynamics in the hamster brain

    Yasutaka Mukai, Jumpei Kuroda, Riho Kobayashi, Yumin Zhang, Ren Y Sato, Hiroaki Norimoto

    NEURO2024  2024.7.26 

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KAKENHI (Grants-in-Aid for Scientific Research) 4

  1. Unraveling the molecular basis of "yawning" in the brain

    Grant number:24K18232  2024.4 - 2027.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

  2. Physiological role of sustained suppression of neural activity by prostaglandin E2

    Grant number:22K15225  2022.4 - 2024.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Early-Career Scientists

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    Authorship:Principal investigator 

    Grant amount:\4680000 ( Direct Cost: \3600000 、 Indirect Cost:\1080000 )

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  3. Physiological role of long-lasting suppression of noradrenergic neurons in the locus coeruleus induced by prostaglandin E2

    Grant number:21K20688  2021.8 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Research Activity Start-up

    Mukai Yasutaka

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    Authorship:Principal investigator 

    Grant amount:\3120000 ( Direct Cost: \2400000 、 Indirect Cost:\720000 )

    When experiencing stress, one may feel “malaise” for several hours to several days. Could one of the causes be the “long-lasting neural activity changes” that occur only during this time period? Noradrenergic neurons in the locus coeruleus (LC-NA neurons) are involved in the regulation of attention and sleep/wakefulness. Prostaglandin E2 (PGE2) is involved in the stress responses induced by both physical and psychological stressors. Previously, it was found that PGE2 induces long-lasting suppression of the activity of LC-NA neurons via EP3 receptor in acute brain slices. In this study, functional roles of the long-lasting suppression was examined in vivo, using conditional knockout mice of EP3 receptor in NA neurons. The results suggested that EP3-mediated suppression of the activity of noradrenergic neurons would be involved in the suppression of depression-like behavior and inhibition of wakefulness after psychological stress exposure.

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  4. The function of neuromodulation of hypothalamic neurons for switching of sleep-wakefulness

    Grant number:18J21665  2018.4 - 2021.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for JSPS Fellows  Grant-in-Aid for JSPS Fellows

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