Faculty Profiles - MUKAI Yasutaka

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

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Degree 3

Doctor (Medicine) （ 2021.3 Nagoya University ）
Master (Medical Science) （ 2017.3 Nagoya University ）
Bachelor (Science) （ 2015.3 Nagoya University ）

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Research Areas 5

Life Science / Molecular biology
Life Science / Physiology
Life Science / Neuroscience-general
Life Science / Pharmacology
Life Science / Function of nervous system

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Research History 6

Nagoya University Graduate School of Science Assistant Professor

2024.9
Nagoya University Neuroethology Group, Graduate School of Science

2024.9

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Nagoya City University Graduate School of Pharmaceutical Sciences Department of Neuropharmacology

2024.4 - 2024.8

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Hokkaido University Department of Cellular Pharmacology, Graduate School of Medicine

2023.4 - 2024.3

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Country：Japan

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Nagoya University Research Institute of Environmental Medicine

2015.4 - 2023.3

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Nagoya University School of Science, Department of Biological Science

2014.4 - 2015.3

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Education 3

Nagoya University Graduate School of Medicine Doctoral Course in Integrated Medicine

2017.4 - 2021.3

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Nagoya University Graduate School of Medicine Master's Course in Medical Science

2015.4 - 2017.3

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Country： Japan

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Nagoya University School of Science Department of Biological Science

2011.4 - 2015.3

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Professional Memberships 2

The Physiological Society of Japan

2016.11
The Japan Neuroscience Society

2016.1

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Awards 4

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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Best Poster Prize

2018.11

Yasutaka Mukai

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Poster Prize

2018.9 Cold Spring Harbor Laboratory Meeting “Molecular Mechanisms of Neural Connectivity” Molecular mechanisms underlying long-lasting calcium increase in orexin neurons by dopamine

Yasutaka Mukai

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Poster Prize

2018.2 The 10th NAGOYA Global Retreat Physiological role of long‒lasting calcium increase in orexin neurons by dopamine

Yasutaka Mukai

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Papers 13

Prostaglandin E2Induces 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 Language：English 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 ([Ca2+]i) 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 [Ca2+]i, and pancreatic polypeptide and prostaglandin D2, which decrease [Ca2+]i. Among them, neuromedin U induced the greatest response in female mice. In terms of the duration of [Ca2+]ichange, we focused on prostaglandin E2(PGE2), since it induces a long-lasting decrease in [Ca2+]ivia the EP3receptor. Conditional knock-out of the receptor in LC-NA neurons resulted in increased depression-like behavior, prolonged wakefulness in the dark period, and increased [Ca2+]iafter 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 E2can 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 E2(PGE2) 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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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 Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

DOI： 10.1016/j.neures.2022.12.009

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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 ) page： 3966 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
Identification of substances which regulate activity of corticotropin-releasing factor-producing neurons in the paraventricular nucleus of the hypothalamus. Reviewed International journal

Yasutaka Mukai, Ayako Nagayama, Keiichi Itoi, Akihiro Yamanaka

Scientific reports Vol. 10 ( 1 ) page： 13639 - 13639 2020.8

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Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)

The stress response is a physiological system for adapting to various internal and external stimuli. Corticotropin-releasing factor-producing neurons in the paraventricular nucleus of the hypothalamus (PVN-CRF neurons) are known to play an important role in the stress response as initiators of the hypothalamic-pituitary-adrenal axis. However, the mechanism by which activity of PVN-CRF neurons is regulated by other neurons and bioactive substances remains unclear. Here, we developed a screening method using calcium imaging to identify how physiological substances directly affect the activity of PVN-CRF neurons. We used acute brain slices expressing a genetically encoded calcium indicator in PVN-CRF neurons using CRF-Cre recombinase mice and an adeno-associated viral vector under Cre control. PVN-CRF neurons were divided into ventral and dorsal portions. Bath application of candidate substances revealed 12 substances that increased and 3 that decreased intracellular calcium concentrations. Among these substances, angiotensin II and histamine mainly increased calcium in the ventral portion of the PVN-CRF neurons via AT1 and H1 receptors, respectively. Conversely, carbachol mainly increased calcium in the dorsal portion of the PVN-CRF neurons via both nicotinic and muscarinic acetylcholine receptors. Our method provides a precise and reliable means of evaluating the effect of a substance on PVN-CRF neuronal activity.

DOI： 10.1038/s41598-020-70481-5

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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 ) page： pgae275 2024.6

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Language：English 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
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 ) page： 22 2024.5

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Language：English 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 (ovBNSTCRF 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 ovBNSTCRF 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
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 ) page： e2301951120 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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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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Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

DOI： 10.1016/j.cub.2023.07.013

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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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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 (VTAGad67+) 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 VTAGad67+ 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 VTAGad67+ 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 (DRN5–HT) were monosynaptically innervated and inhibited by VTAGad67+ neurons. All recorded DRN5–HT neurons received inhibitory input from VTAGad67+ neurons, while only one quarter of them received inhibitory input from local GABAergic neurons. Gad67+ neurons in the DRN (DRNGad67+) also received monosynaptic inhibitory input from VTAGad67+ neurons. Taken together, we found that VTAGad67+ neurons were integrated in many inputs, and their output inhibits DRN5–HT neurons, which may regulate physiological functions including sleep/wakefulness.

DOI： 10.3389/fnins.2022.877054

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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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The mammalian circadian pacemaker regulates wakefulness via CRF neurons in the paraventricular nucleus of the hypothalamus. Reviewed International journal

Daisuke Ono, Yasutaka Mukai, Chi Jung Hung, Srikanta Chowdhury, Takashi Sugiyama, Akihiro Yamanaka

Science advances Vol. 6 ( 45 ) 2020.11

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In mammals, the daily rhythms of physiological functions are timed by the central circadian clock located in the suprachiasmatic nucleus (SCN) of the hypothalamus. Although the importance of the SCN for the regulation of sleep/wakefulness has been suggested, little is known about the neuronal projections from the SCN, which regulate sleep/wakefulness. Here, we show that corticotropin-releasing factor (CRF) neurons in the hypothalamic paraventricular nucleus mediate circadian rhythms in the SCN and regulate wakefulness. Optogenetic activation of CRF neurons promoted wakefulness through orexin/hypocretin neurons in the lateral hypothalamus. In vivo Ca2+ recording showed that CRF neurons were active at the initiation of wakefulness. Furthermore, chemogenetic suppression and ablation of CRF neurons decreased locomotor activity and time in wakefulness. Last, a combination of optical manipulation and Ca2+ imaging revealed that neuronal activity of CRF neurons was negatively regulated by GABAergic neurons in the SCN. Our findings provide notable insights into circadian regulation of sleep/wakefulness in mammals.

DOI： 10.1126/sciadv.abd0384

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REM sleep–active MCH neurons are involved in forgetting hippocampus-dependent memories Reviewed International journal

Shuntaro Izawa, Srikanta Chowdhury, Toh Miyazaki, Yasutaka Mukai, Daisuke Ono, Ryo Inoue, Yu Ohmura, Hiroyuki Mizoguchi, Kazuhiro Kimura, Mitsuhiro Yoshioka, Akira Terao, Thomas S. Kilduff, Akihiro Yamanaka

Science Vol. 365 ( 6459 ) page： 1308 - 1313 2019.9

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Language：English Publishing type：Research paper (scientific journal) Publisher：American Association for the Advancement of Science ({AAAS})

The neural mechanisms underlying memory regulation during sleep are not yet fully understood. We found that melanin concentrating hormone-producing neurons (MCH neurons) in the hypothalamus actively contribute to forgetting in rapid eye movement (REM) sleep. Hypothalamic MCH neurons densely innervated the dorsal hippocampus. Activation or inhibition of MCH neurons impaired or improved hippocampus-dependent memory, respectively. Activation of MCH nerve terminals in vitro reduced firing of hippocampal pyramidal neurons by increasing inhibitory inputs. Wake- and REM sleep-active MCH neurons were distinct populations that were randomly distributed in the hypothalamus. REM sleep state-dependent inhibition of MCH neurons impaired hippocampus-dependent memory without affecting sleep architecture or quality. REM sleep-active MCH neurons in the hypothalamus are thus involved in active forgetting in the hippocampus.

DOI： 10.1126/science.aax9238

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Books 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 50

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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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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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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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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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

Language：English Presentation type：Poster presentation

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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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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

Language：English Presentation type：Poster presentation

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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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Prostaglandin E2 induces long-lasting calcium decrease of noradrenergic neurons in the locus coeruleus

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

The 43rd Annual Meeting of the Japan Neuroscience Society 2020.7.29

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Event date： 2020.7 - 2020.8

Language：English Presentation type：Poster presentation

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Long-lasting calcium increase is induced by dopamine via D1 receptor in hypothalamic orexin neurons

Yasutaka Mukai, Hidenori Aizawa, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

The 97th Annual Meeting of The Physiological Society of Japan 2020.3.17

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Event date： 2020.3

Language：English Presentation type：Poster presentation

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Dopamine induces long-lasting increase of intracellular calcium in orexin neurons in the hypothalamus via D1 receptor

Yasutaka MUKAI

The 1st CIBoG Retreat (The 12th NAGOYA Global Retreat) 2020.2.7

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Event date： 2020.2

Language：English Presentation type：Poster presentation

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Long-lasting calcium increase via dopamine D1 receptor in orexin neurons of the hypothalamus

Yasutaka Mukai, Hidenori Aizawa, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

2019.10.17

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Event date： 2019.10

Language：Japanese Presentation type：Poster presentation

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Dopamine induces long-lasting increase of intracellular calcium in orexin neurons in the hypothalamus

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

Opto2019 2019.9.11

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Event date： 2019.9

Language：English Presentation type：Poster presentation

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Identification of receptors implicated in modulation of activity of orexin neurons by genome editing

Yasutaka MUKAI

2019.8.23

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Event date： 2019.8

Language：Japanese Presentation type：Oral presentation (general)

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Dopamine induced long-lasting calcium increase in orexin neurons via dopamine D1 receptor

Yasutaka Mukai, Hidenori Aizawa, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

Neuro2019 2019.7.25

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Event date： 2019.7

Language：English Presentation type：Poster presentation

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Dopamine induced long-lasting calcium increase in orexin neurons via D1-like receptor

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

9th FAOPS congress 2019.3.30

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Event date： 2019.3

Language：English Presentation type：Poster presentation

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Long-lasting calcium increase induced by dopamine in orexin neurons via D1-like receptor

Yasutaka MUKAI

The 11th NAGOYA Global Retreat 2019.2.15

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Event date： 2019.2

Language：English Presentation type：Poster presentation

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Long-lasting intracellular calcium increase by dopamine in orexin neurons of the hypothalamus

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

2018.11.22

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Event date： 2018.11

Language：Japanese Presentation type：Poster presentation

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Molecular mechanisms underlying long-lasting calcium increase in hypothalamic orexin neurons by dopamine

Yasutaka MUKAI

The 6th Neural Circuits Joint Workshop 2018.10.5

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Event date： 2018.10

Language：English Presentation type：Oral presentation (general)

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Molecular mechanisms underlying long-lasting calcium increase in orexin neurons by dopamine International conference

Yasutaka Mukai

Cold Spring Harbor Laboratory Meeting “Molecular Mechanisms of Neural Connectivity” 2018.9.27

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Event date： 2018.9

Language：English Presentation type：Poster presentation

Venue：Cold Spring Harbor Laboratory, NY Country：United States

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Seconds-to-hours-scale neuromodulation in the hypothalamus

Yasutaka MUKAI

2018.8.23

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Event date： 2018.8

Language：Japanese Presentation type：Oral presentation (general)

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Screening of substances modulating activity of CRF neurons in the hypothalamus

Yasutaka Mukai, Ayako Nagayama, Takeharu Nagai, Keiichi Itoi, Akihiro Yamanaka

The 41st Annual Meeting of the Japan Neuroscience Society 2018.7.28

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Event date： 2018.7

Language：English Presentation type：Poster presentation

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Physiological role of long-lasting intracellular calcium increase in orexin neurons by dopamine

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

The 95th Annual Meeting of The Physiological Society of Japan 2018.3.30

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Event date： 2018.3

Language：English Presentation type：Poster presentation

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Physiological role of long-lasting intracellular calcium increase in orexin neurons by dopamine

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

2018.3.27

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Event date： 2018.3

Language：Japanese Presentation type：Oral presentation (general)

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Physiological role of long‒lasting calcium increase in orexin neurons by dopamine

Yasutaka MUKAI

The 10th NAGOYA Global Retreat 2018.2.16

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Event date： 2018.2

Language：English Presentation type：Poster presentation

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Identification of neural circuits projecting from the hypothalamus to the hippocampus

Yasutaka MUKAI

2017.12.20

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Event date： 2017.12

Language：Japanese Presentation type：Poster presentation

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Analysis of long-lasting effect of dopamine on hypothalamic orexin neurons

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

ConBio2017 2017.12.7

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Event date： 2017.12

Language：English Presentation type：Oral presentation (general)

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Elucidating the function of neuromodulation in the hypothalamus for sleep-wakefulness switching

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

2017.11.28

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Event date： 2017.11

Language：Japanese Presentation type：Oral presentation (general)

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Long-lasting effect of dopamine on hypothalamic orexin neurons

Yasutaka MUKAI

The 5th Neural Circuits Joint Workshop 2017.9.22

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Event date： 2017.9

Language：English Presentation type：Oral presentation (general)

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Analysis of long-lasting effect of bioactive molecules on specific neurons by calcium imaging in brain slice

Yasutaka MUKAI

2017.9.6

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Event date： 2017.9

Language：Japanese Presentation type：Poster presentation

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Long lasting effect of dopamine on hypothalamic orexin neurons

Yasutaka MUKAI

2017.8.29

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Event date： 2017.8

Language：Japanese Presentation type：Oral presentation (general)

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Screening of substances affect MCH neurons and orexin neurons by calcium-imaging in mouse acute brain slice

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

The 40th Annual Meeting of the Japan Neuroscience Society 2017.7.21

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Event date： 2017.7

Language：English Presentation type：Poster presentation

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Identification of substances affect MCH neurons and orexin neurons by calcium imaging screening

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

The 94th Annual Meeting of The Physiological Society of Japan 2017.3.28

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Event date： 2017.3

Language：English Presentation type：Poster presentation

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Screening of Factors Regulate Noradrenergic Neurons in the Locus Coeruleus by Calcium-Imaging in Mouse Acute Brain Slice

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

The 1st ABiS Symposium 2017.2.19

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Event date： 2017.2

Language：English Presentation type：Poster presentation

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Identification of substances affect the activity of MCH neurons and orexin neurons by calcium imaging screening system

Yasutaka MUKAI

The 9th NAGOYA Global Retreat 2017.2.10

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Event date： 2017.2

Language：English Presentation type：Poster presentation

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Identification of factors regulate activity of specific type of neurons by calcium-imaging Invited

Yasutaka MUKAI

2016.12.26

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Event date： 2016.12

Language：Japanese Presentation type：Oral presentation (general)

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Identification of hypothalamic neuron types projecting to hippocampus by retrograde tracers

Yasutaka Mukai, Akihiro Yamanaka

2016.11.2

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Event date： 2016.11

Language：Japanese Presentation type：Poster presentation

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Screening of factors regulating activity of MCH and orexin neurons using calcium imaging

Yasutaka Mukai, Azusa Inui, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

2016.10.14

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Event date： 2016.10

Language：Japanese Presentation type：Oral presentation (general)

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Screening of factors which affect noradrenergic neurons in the locus coeruleus by calcium-imaging in mouse acute brain slice

Yasutaka MUKAI

The 4th Neural Circuits Joint Workshop 2016.10.7

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Event date： 2016.10

Language：Japanese Presentation type：Oral presentation (general)

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Screening of factors affect noradrenergic neurons in the locus coeruleus by calcium-imaging in mouse acute brain slice

Yasutaka MUKAI

2016.9.30

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Event date： 2016.9

Language：Japanese Presentation type：Poster presentation

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Screening of substances which affect noradrenergic neurons in the locus coeruleus by calcium imaging in mouse acute brain slice

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

2016.9.23

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Event date： 2016.9

Language：Japanese Presentation type：Poster presentation

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Screening of substances affect noradrenergic neurons in the locus coeruleus using tetO YC-Nano mice

Yasutaka MUKAI

2016.8.30

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Event date： 2016.8

Language：Japanese Presentation type：Oral presentation (general)

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Screening of substances affect noradrenergic neurons in the locus coeruleus by calcium-imaging in mouse acute brain slice

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

The 39th Annual Meeting of the Japan Neuroscience Society 2016.7.20

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Event date： 2016.7

Language：English Presentation type：Poster presentation

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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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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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Presentation type：Poster presentation

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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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Presentation type：Poster presentation

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Screening of substances affect noradrenergic neurons in the locus coeruleus by calcium-imaging

Yasutaka Mukai, Chowdhury Srikanta, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

The 8th NAGOYA Global Retreat 2016.2.12

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Identification of input pathway of noradrenargic neurons in the locus coeruleus using calcium imaging

Yasutaka Mukai, Chowdhury Srikanta, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

2015.12.18

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Language：Japanese Presentation type：Poster presentation

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Identification of input/output pathways of specific neuron populations using TetO YC-Nano mice

Yasutaka MUKAI

2015.9.1

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Screening of substances affect noradrenergic neurons in the locus coeruleus by calcium-imaging

Yasutaka Mukai, Chowdhury Srikanta, Kenji F Tanaka, Takeharu Nagai, Akihiro Yamanaka

International Symposium on Adaptive Circuit Shift 2016 (ACS2016) 2016.3.3

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To the head of Presentations.▲

KAKENHI (Grants-in-Aid for Scientific Research) 5

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 ）
Unraveling the neural mechanisms of "yawning"

Grant number：23KJ0002 2023.4 - 2026.3

Grants-in-Aid for Scientific Research Grant-in-Aid for JSPS Fellows

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Authorship：Principal investigator

Grant amount：\4680000 （ Direct Cost: \3600000 、 Indirect Cost：\1080000 ）
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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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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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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To the head of KAKENHI (Grants-in-Aid for Scientific Research).▲