The 7th Annual

IIIS Symposium~ Solving the mystery of sleep ~

Date
Venue

: Thursday, December 20, 2018
: Tokyo Conference Center Shinagawa

The 7th Annual IIIS Symposium~ Solving the mystery of sleep ~December 20, 2018
Tokyo Conference Center Shinagawa
Tokyo, Japan

Organizer

Masashi Yanagisawa
International Institute for Integrative Sleep Medicine (WPI-IIIS)
University of Tsukuba

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Opening
Director, WPI-IIIS, University of Tsukuba

Opening Address 1

Masashi Yanagisawa
Akira Ukawa

Opening Address 2

Tadatoshi Kaneko

Director of Office for Basic Research Programs,
Basic Research Promotion Division (MEXT)

Welcome10:00 - 10:15

WPI Program Director

Session 1 | Chair: Yo Oishi
10:15 - 10:45

Neurochemincal mechanisms of
post-training processing inperceptual learning

Takeo Watanabe

Brown University

Page. 4

10:45 - 11:15

Genetic and circuit analysis of
empathy behaviors in the mouse

Hee-Sup Shin

Center for Cognition and Sociality,
Institute for Basic Science

Page. 5

11:15 - 11:45

The interaction between sleep andAkiko Satohaging mediated by DMH neurons

National Center for
Geriatrics and Gerontology

Page. 6

11:45 - 12:15

Break & Lunch preparation

WILLDYNAMICS Luncheon Session | Chair: Takeshi Sakurai
12:15 - 12:45

Motivated behavior regulated by
the ventral striatum

Kenji Tanaka

Keio University

Page. 7

12:45 - 13:15

How do mice detect and escapefrom their predator?

Peng Cao

National Institute of Biological Sciences,
Beijing

Page. 8

Gunma University

Page. 9Poster Session & Tea Break | Chair: Michael Lazarus
13:15 - 14:15

Data Blitz and Poster Presentation

Session 2 | Chair: Kaspar Vogt
14:15 - 14:45

Multiscale understanding ofsynaptic pathology of psychiatricdisorders

14:45 - 15:15

Balancing brain plasticity/stability Takao Hensch

Harvard Medical School /Harvard University /WPI-IRCN, The University of Tokyo

Page. 10

15:15 - 15:45

Neural ensemble dynamics during
Tomomi Tsunematsu
REM sleep and P-waves in mice

Tohoku University

Page. 11

15:45 - 16:00

Break / Photo

Akiko Hayashi-Takagi

MSD Afternoon Seminar | Chair: Masashi Yanagisawa
16:00 - 16:30

Neural circuitry of sleepiness andThomas E. Scammell
cataplexy in narcolepsy

Beth Israel Deaconess Medical Center /Harvard Medical School

Page. 13

16:30 - 17:00

Identification of neurons
regulating REM/non-REM sleep
Yu Hayashi
and insights to the mechanisms of
REM sleep behavior disorder

WPI-IIIS, University of Tsukuba

Page. 1417:00 - 17:30

Neuron-glia metabolic coupling :role in neuronal plasticity,
Pierre J. Magistretti
neuroprotection and regulation
across the sleep-wake cycle

King Abdullah University of Science andTechnology /École Polytechnique Fédérale dePage. 15
Lausanne /Département de Psychiatrie, UNILCHUV, Site de Cery

17:30

Closing

18:00 - 20:00

Reception!

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1. No outlets are available nearby audience seats
2. No smoking in symposium venues: please smoke at the designated area on each floor
3. Wireless LAN is available in the foyer.

/-",0Free lunch will be provided for pre-registered participants.

1+,+2()$"
18:00 - 20:00 at Foyer on 5th floor
For MSD afternoon seminar attendees.

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45678497

Takeo Watanabe
Brown University, USA"#$%&'#%())*+,%---.%./01234*0!

After encoding of learning, its state changes through several
different stages. We examined post-training stages of visual
perceptual learning (VPL; Watanabe et al, Nature, 2001 &2003; Tsushima et al, 2006, Science; Shibata et al, 2011,
Science). Particularly, we have addressed the questions of
how VPL is stabilized after training and also how consolidated VPL is re-stabilized after reactivation. Inspired by a series
of work by Dr. Takao Hensch and his colleagues on a animal
visual critical period (Morishita & Hensch, 2008, Curr Opin
Neurobiol), we measured the concentration of glutamate, an
excitatory neurotransmitter, divided by the concentration of
GABA, an inhibitory neurotransmitter (E/I ratio) in humanvisual areas using magnetic resonance spectroscopy at different post-encoding stages of VPL. First, we examined overlearning that refers to a learning state resulting from continuous training after the saturation of performance increases. We
found that overlearned VPL interfered with subsequent learning of a new task (anterograde interference). In this case,overlearning was accompanied with rapid and abrupt
decrease in E/I ratios from higher to lower than baselines.
Second, we found that if training was terminated before thesaturation of performance increase, VPL of the trained task
was interfered with by subsequent training on a new task
(retrograde interference) and that an E/I ratio was higher 30
min after the training than baselines and then decreased tothe baselines 3.5 hours later (Shibata et al, 2017, Nat Neurosci). Third, after encoding and consolidation of learning of atask, performance of a handful of trials of the task made a VPL
state subject to retrograde interference (reactivation) and E/Iratio changes after the reactivation were highly similar to
those after encoding. This suggests similar aspects of mechanisms between the states after encoding and reactivation of
VPL (Bang et al, 2018, Nat Hum Behav).

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6789:6;9Hee-Sup Shin
Center for Cognition andSociality, Institute for Basic
Science, Korea

Unraveling neural mechanisms underlying social behaviors
is one of the major subjects in neuroscience. Diverse tools
recently developed for doing experiments in rodents allow
multidisciplinary studies on such subjects from molecules tosystems. Empathy, the capacity to recognize and shareemotions with others, is crucial for our social interaction andmental well-being. This ability is conserved from rodents tohumans, and the anterior cingulate cortex (ACC) is known to
be integral in the acquisition of observational fear, a rodent
model of empathic fear. Despite the fundamental importanceof genetic factors underlying individual variability inempathy-related behaviors, molecular and cellularmechanisms in the ACC that control observational fear (OF)remain to be determined. Through examining several mutant
strains for OF behavior as well as through behavior-driven
forward genetic analyses, we found several gene mutations
that influence OF behavior in the mouse. One of them, amissense mutation in Nrxn3, causes an increase inobservational fear. Using a combination of tools we findevidence that Nrxn3 is an essential molecule for inhibitory
synaptic transmission in SST-positive neurons, and uncover a
novel role of SST interneurons in the ACC in gating the
top-down computation for the expression of socially incitedfear.

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Akiko Satoh
National Center for Geriatrics
and Gerontology, Japan"#$%&'#%())*+,%---.%./01234*0!

Aging has significant impacts on sleep, resulting in increases
in sleep fragmentation and sleep onset latency, and adecrease in sleep quality in mammals. We have recently
found that diet restriction (DR), a dietary regimen
well-known to delay the aging process and to extend lifespanin a wide variety of organisms including mammals, candramatically attenuate some of age-associated sleep
alterations. For example, DR significantly reduces the level ofage-associated sleep fragmentation. Therefore, DR may delay
the aging process and extend lifespan by critically altering
sleep control in aged animals.
To further elucidate mechanisms by which DR ameliorates
age-associated sleep alterations, we focus on the gene called
PR-domain containing factor 13 (PRDM13). PRDM13 is a
SIRT1 downstream gene and is exclusively expressed in thedorsomedial hypothalamus (DMH). The DMH has beenshown to control age-associated physiological changes andlongevity through SIRT1. Mice with knockdown of Prdm13 in
the DMH display reduced NREM delta power. In addition,
DMH-specific Prdm13-knockdown mice display defect insleep homeostasis, but not in circadian clock. As well as
Prdm13-knockdown mice, DMH-specific Sirt1-knockdown
mice also display reduced NREM delta power. These findings
suggest that the DMH contributes to modulate quality ofsleep through maintaining sleep homeostasis by the
SIRT1/PRDM13 axis during the aging process. In this talk, I
will discuss about a role of DMH neurons on age-associatedsleep alterations. I will also propose how poor sleep quality
promotes the age-associated pathophysiology in peripheralorgans/tissues and ultimately affects longevity.

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45678497

Kenji Tanaka
Keio University, JapanThe assessment of motivation is highly subjective, owing to
the variety of psychological conception of motivation. To
improve the objectivity of motivation, it has been proposedthat the level of motivation is addressed by the quantitative
consequences of the goal-directed behavior. The
goal-directed behavior comprises of action selection, action
initiation, and action sustainment to pursue the goal. Eachdomain is regulated by the cortico-striatal circuit and theventral striatum is known to be a key node of this behavior.
Recent animal studies demonstrated that the ventromedial
part of the striatum controls the action selection, and theventrolateral striatum regulates action initiation. However,
little is known about how the ventral striatum is involved in
the action sustainment. We will talk about the neuralsubstrate mediating action sustainment and will discuss theinvolvement of the ventral striatum in the goal-directedaction sustainment.
Ref:
1. Tsutsui-Kimura et al., Distinct roles of ventromedial
versus ventrolateral striatal medium spiny neurons inreward-oriented behavior. Current Biology,27(19):3042-3048, 20172.

Natsubori et al., Ventrolateral Striatal Medium Spiny
Neurons Positively Regulate Food-Incentive,
Goal-Directed Behavior Independently of D1 and D2
Selectivity. J Neurosci. 37(10):2723-2733, 20173.

Tsutsui-Kimura et al., Dysfunction of ventrolateral striatal
dopamine receptor type 2-expressing medium spiny
neurons impairs instrumental motivation. Nat Commun
8: 14304, 2017"#$%!&#%'(()*+%,,,-%-./0123)/!

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34567386

Peng Cao
National Institute of Biological
Sciences, Beijing, China"#$%&'#%())*+,%---.%./01234*0!

The innate defensive behaviors in response to environmental
threats play a fundamental role in survival. However, little is
known about the neural circuits specifically processing
threat-relevant sensory information in the mammalian brain.
We identified parvalbumin-positive (PV+) excitatory projection neurons in mouse superior colliculus (SC) as a key neuronal subtype for detecting looming visual objects. These
neurons, distributed predominantly in the retinal-recipientlayers of the SC, are both necessary and sufficient to trigger
dimorphic defensive behaviors, i.e. escape and freezing. Two
distinct groups of SC PV+ neurons form divergent pathways
to transmit threat-relevant visual signals to neurons in theparabigeminal nucleus (PBGN) and lateral posterior thalamic
nucleus (LPTN). Activations of PV+ SC-PBGN and SC-LPTN
pathways mimic the dimorphic defensive behaviors. Bilateralinactivation of either nucleus results in the defensive behavior dominated by the other nucleus. Together, these datasuggest that the SC PV+ neurons, as a key neuronal subtype
to detect looming visual objects, orchestrates dimorphic
defensive behaviors with two mutually competitive tectofugal pathways that may operate in a "winner-take-all" process.

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45678497

Akiko Hayashi-Takagi
Gunma University, Japan

Various lines of evidence have suggested that synaptopathy is
involved in schizophrenia. However, it is unknown whether
synaptopathy is an underlying mechanism of disease or asecondary consequence. Thus, we performed a longitudinalin vivo 2-photon imaging analysis of the brain of a schizophrenia model (DISC1 knockdown mice) and found that thismodel exhibited a decrease in the density of dendritic spines,
where the majority of excitatory synapses are formed.
Furthermore, we found a significantly greater number oflarge dendritic spines in the model mice. The presence of thelarge spines in the schizophrenia mice model mirrors findings from another schizophrenia mice model, calcineurinknockout mice. It is well-known that there is a strong correlation between spine head size and its synaptic efficacy, whereby the large spines can generate a larger synaptic current.
This led us to hypothesize that large spines can non-linearlyaffect the dendritic computation, causally resulting in subsequent behavioral alterations. To test this hypothesis, we use a
multiscale analysis that consists of an uncaging-evokedsingle spine EPSC measurement and Ca2+ imaging to visualize the synaptic input, dendritic event, action potential, andbehavioral manifestations. In addition, with use of in vivo
optical and in silico manipulation of the spines in the model
animals, we are now trying to causally examine what kind ofsynaptic pathology would underlie the pathology of disorders.

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Takao Hensch
Harvard Medical School, USA /Harvard University, USA /WPI-IRCN, The University ofTokyo, Japan#$%&'($&)**+,-&.../&/012345+1!"

Brain function is largely shaped by experience in early life,
creating windows of both great opportunity and vulnerability.
Our work has focused on the biological basis for such critical
periods, identifying both “triggers” and “brakes” on plasticity.
Strikingly, the maturation of particular inhibitory circuits ispivotal for the onset timing of these windows. Manipulationsof their emergence can either accelerate or delay
developmental trajectories regardless of chronological age.
Notably, many neurodevelopmental disorders are linked toalterations in excitatory-inhibitory balance, suggesting
shifted critical period timing as part of their etiology. Closureof critical periods in turn reflects an active process, rather
than a purely passive loss of plasticity factors. Lifting thesebrakes allows the reopening of plastic windows later in life,
but may also underlie instability in disease states. Thus,
understanding how brain plasticity and stability are balanced
throughout life offers new insight into mental illness andnovel therapeutic strategies for recovery of function in
adulthood.

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Tomomi Tsunematsu
Tohoku University, Japan

Rapid eye movement (REM) sleep is characterized by hippocampal theta waves and phasic sub-second waves in thebrainstem, so-called ponto-geniculo-occipital (PGO) waves
in cats or pontine (P) waves in rodents. The sub-second pontine wave during REM sleep was originally described in the
1960s. Hobson and colleagues have proposed that P-waves
construct the hallucinoid visual imagery of dreams. However, we still do not know the biological function of P-waves
and also occurrence of P-waves in mice. In this study, weinvestigated the temporal evolution of P-waves and underlying neural ensemble dynamics in the brainstem. First, toexamine how P-waves appear during the sleep-wake cycle,
bipolar electrodes were implanted into the sublaterodorsal
nucleus (SLD) of head-fixed mice. The density of P-waves was
typically at ~ 0.8 Hz during REM sleep, consistent with thatin cats and rats. Second, to monitor neural ensemble dynamics during P-wave, we inserted a 4-shank silicon probe tocover multiple brainstem nuclei simultaneously. While a rich
structure of neural activity was apparent across brainstem
nuclei, we found that P-waves during REM sleep were associated with highly synchronous burst firing across nuclei. Next,
we also investigated functional interactions between thebrainstem and hippocampus during P-wave genesis. WhileP-waves were seen during both REM and non-REM sleep, thefunctional connectivity between two structures was changed
depending on sleep states. Our findings suggest that P-waves
involve in state-dependent coordinated activity across brain
regions.

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Thomas E. Scammell
Beth Israel Deaconess
Medical Center, USA /Harvard Medical School, USA

Narcolepsy is the most common neurological cause ofchronic sleepiness and is caused by selective loss of theorexin neurons. Research suggests that this sleepiness is notdue to higher homeostatic sleep pressure or weak circadianwaking drive, but instead is caused by loss of excitatory
signaling from the orexin neurons onto a variety of wake-promoting brain regions. For example, restoration of orexin
signaling in the histaminergic neurons of the tuberomammillary nucleus substantially improves the ability of mice to stayawake for long periods, and orexin signaling through othermonoaminergic regions is similarly effective. Just whichaspects of arousal are mediated by these pathways is now
under investigation.
Narcolepsy is also characterized by cataplexy – sudden
episode of muscle paralysis usually triggered by strong positive emotions, usually under social circumstances. We foundthat activation of GABAergic neurons of the central nucleusof the amygdala (CeA) increases cataplexy whereas inhibition reduces cataplexy. The CeA contains a great variety ofGABAergic neurons, some mediating responses to positive
stimuli and other mediating fear behaviors. We are now finding that CeA neurons responsive to the pro-social hormone
oxytocin (OT) can strongly drive cataplexy via specificprojections to the brainstem. Defining these pathways helps
identify new targets for narcolepsy treatments, and also helps
identify specific amygdala population that may influence
positive affect of relevance to psychiatric disease.

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Yu Hayashi
WPI-IIIS, University of Tsukuba,Japan#$%&'($&)**+,-&.../&/012345+1!"

Over the night, our sleep cycles between two distinct states,
rapid eye movement (REM) sleep and non-REM sleep.
Abnormal balance of the two sleep states is a common andearly symptom in various neurological disorders, suggestingthat each sleep state plays crucial roles. Little is known,
however, about the individual roles and neural substrates ofthese two states. We applied mouse genetics to functionallydissect neurons in the brainstem and identify neurons
involved in regulating REM/non-REM sleep. With thisapproach, we previously identified glutamatergic and
GABAergic neurons in the pontine tegmental area thatnegatively regulate REM sleep (*). Recently, we further
searched for molecular markers in this brain area that allow
precise manipulation of neuronal subgroups. In one group of
neurons, genetic inhibition led to a drastic decrease in REM
sleep, suggesting that these neurons play an essential role ingenerating REM sleep. Moreover, the mice frequently
exhibited aggressive movements during REM sleep,
resembling REM sleep behavior disorder (RBD). RBD is asleep disorder in which patients act out of their dreams andexhibit violent behavior during REM sleep. We expect thatthese neurons are a key to understanding the neural circuitryof REM/non-REM sleep and that our genetic mouse model
provides important implications about the neuralmechanisms of RBD.
*Hayashi et al., Science 350, 957-961, 2015

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Pierre J. MagistrettiKing Abdullah University of
Science and Technology,
Saudi Arabia/
École Polytechnique Fédérale deLausanne, Switzerland/Département de Psychiatrie,
UNIL-CHUV, Site de Cery,
Switzerland

A tight metabolic coupling between astrocytes and neurons isa key feature of brain energy metabolism (Magistretti andAllaman, Neuron, 2015). Over the years we have described
two basic mechanisms of neurometabolic coupling. First theglycogenolytic effect of VIP and of noradrenaline indicating a
regulation of brain homeostasis by neurotransmitters acting
on astrocytes, as glycogen is exclusively localized in thesecells. Second, the glutamate-stimulated aerobic glycolysis inastrocytes. Both the VIP-and noradrenaline-induced glycogenolysis and the glutamate-stimulated aerobic glycolysis
result in the release of lactate from astrocytes as an energy
substrate for neurons through a process now known as the
Astrocyte-Neuron-Lactate Shuttle (ANLS) (Magistretti andAllaman, Neuron, 2015; Magistretti and Allaman, Nature
Reviews Neuroscience, 2018).
We have shown that lactate is necessary not only as anenergy substrate but is also a signaling molecule forlong-term memory consolidation and for maintenance of LTP(Suzuki et al, Cell, 2011).
At the molecular level we have found that L-lactate stimulates the expression of synaptic plasticity-related genes (Yanget al, PNAS, 2014). This effect is mediated by the L-lactate
potentiation of NMDA receptor-mediated currents and theensuing increases in intracellular calcium (Jourdain et al,
Scientific Reports, 2018) . These results reveal a novel actionof L-lactate as a signaling molecule for neuronal plasticity.
We have also shown that peripheral administration of lactate
exerts antidepressant-like effects in three animal models ofdepression (Carrard et al, Mol.Psy., 2016).
We also investigated the expression of genes associated with
the ANLS specifically in astrocytes following sleep deprivation. Quantitative RT-PCR analysis showed that levels of
Glut1, α-2-Na/K pump, Glt1, and Ldha mRNAs were significantly increased following Total Sleep Deprivation in astrocytes (Petit et al, Sleep, 2013). These results stress the important role of astrocytes in the maintenance of the neurometabolic coupling across the sleep-wake cycle.
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睡眠に悩む世界中の人々にとっての希望の光となる。
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装着感の良い脳波測定デバイス及び AI による睡眠自動ステージングな

波測定ウエアラブルデバ

どの技術開発を行っています。2020 年までに医療機器としての認証を

イスと AI を駆使した自取得し、医療機関向けに睡眠障害の診断支援サービスの提供を開始する予定です。
同時に健康経営に取り組む企業向けや、将来的に一般向けにもサービスを展開していき、睡眠障害を効果的に予防、正しく診断することで、一人ひとりが睡眠で悩むことなく幸せに生活を営める社会を実動解析による睡眠測定
サービスを 2020 年から開始予定。

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The 7th Annual

IIIS Symposium~ Solving the mystery of sleep ~http://wpi-iiis.tsukuba.ac.jp/
Secretariat: International Institute for Integrative Sleep Medicine (WPI-IIIS),
University of Tsukuba
Phone: 029-853-5857 E-mail：wpi-iiis-alliance@ml.cc.tsukuba.ac.jp