Current Trends and Future Directions of Synapse-Circuit Plasticity Research

Meeting Program

Tuesday (9/3)
15:00

-

18:30

Arrival and Hotel Check-In

18:30

-

20:30

Welcome Dinner @ Fuji (reception 18:00-)

Wednesday (9/4)
Welcome and Introduction
9:00

-

9:10

Masanori Murayama, on behalf of meeting organizers
Scott Soderling, on behalf of meeting organizers

Keynote Lecture
9:15

-

10:00

Kaoru Inokuchi (Introduction: Masanori Murayama)

New Molecules in Synaptic plasticity (Chair: Elly Nedivi)
10:00

-

10:30

Takeshi Imai (J)

10:30-11:00

Susumu Tomita (US)

11:00

-

11:20

Coffee/Tea break

11:20

-

11:50

Mineko Kengaku (J)

11:50

-

12:20

Scott Soderling (US)Luncheon seminar (Sponsor: NIKON INSTECH CO., LTD.)
12:40

-

13:40

Keisuke Ota (J)Masako Ino (NIKON INSTECH CO., LTD.)

New concepts of synaptic plasticity in neural circuit function (Chair: Takeshi Imai)
14:00

-

14:30

Schuichi Koizumi (J)

14:30

-

15:00

Tetsuya Takano (US)

15:00

-

15:30

Haruhiko Bito (J)

15:30

-

15:50

Coffee/Tea break

15:50

-

16:20

Thomas Blanpied (US)

16:20-16:50

Masanori Murayama (J)

17:00

-

18:20

Poster Session and Discussion @ Kaede

18:40

-

20:00

Dinner @ Mugibatake restaurant

20:10

-

22:00

Poster Session and Discussion (Optional)

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Current Trends and Future Directions of Synapse-Circuit Plasticity Research

Thursday (9/5)
8:45

-

8:55

Welcome and solicitation of feedback for next day
Masanori Murayama and Scott Soderling

Keynote Lecture
9:00

-

9:45

Richard Mooney (Introduction: Scott Soderling)

New concepts of synaptic plasticity in disease (Chair: Matthew Kennedy)

9:45

-

10:15

Akiko Hayashi-Takagi (J)10:15

-

10:45

Gavin Rumbaugh (US)

10:45

-

11:05

Coffee/Tea breakNovel and emerging imaging methods for synaptic analysis (Chair: Akiko Hayashi-Takagi)

11:05

-

11:35

Hideji Murakoshi (J)

11:35

-

12:05

Makoto Higuchi (J)

12:05

-

12:35

Takuya Takahashi (J)Luncheon seminar (Sponsor: Olympus Corporation)
12:55

-

13:55

Shinichiro Tsutsumi (J)Kazuhiko Hosono (Olympus Corporation)
New ideas in dynamics of synaptic signaling and structure (Chair: Hideji Murakoshi)

14:00

-

14:30

Elly Nedivi (US)

14:30

-

15:00

Shigeo Okabe (J)

15:00

-

15:30

Lin Tian (US)

15:30

-

16:00

Yukiko Gotoh (J)

16:20

Coffee/Tea break

16:00

New faces in synaptic neuroscience: Trainee talks (Chair: Masanori Murayama)

16:20

-

16:35

Kareem Abdou (J)

16:35

-

16:50

Dalila Ordonez (US)

16:50

-

17:05

PinWu Liu (J)

17:05

-

17:20

Austin M Ramsey (US)

17:20

-

17:35

Daichi Kawaguchi (J)

17:35

-

17:50

Nerea Llamosas (US)P6

Current Trends and Future Directions of Synapse-Circuit Plasticity Research

18:00-18:55

Poster Session and Discussion @ Kaede19:00

-

21:00

Dinner @ Fuji (PIs vote for poster awards)

21:10

-

22:00

Poster Session and Discussion (Optional)

Friday (9/6)
New ideas in pre and postsynaptic function (Chair: Lin Tian)

9:00

-

9:30

Yasunori Hayashi (J)

9:30

-

10:00

Jason Shepherd (US)

10:00

-

10:30

Takeshi Sakaba (J)

10:30

-

10:50

Coffee/Tea break

10:50

-

11:20

Michisuke Yuzaki (J)

11:20

-

11:50

Matthew Kennedy (US)Luncheon seminar (Sponsor: Thorlabs Japan Inc.)
12:00

-

13:00

Henry Haeberle (Thorlabs, Inc.)

13:10

-

13:25

Poster Award (3 persons)

13:25-General discussion and organization of collaborations
Departure of participants
Organizer meeting to draft summary document

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Abstracts
Oral Presentation

P10

Cell ensemble mechanisms underlying memory formation
K. Inokuchi

Memories are not stored in isolation from other memories but are integrated into associative
networks. At the same time, each memory has its own identity. Because association of related
memories, with keeping the identity of each memory, is the fundamentals of knowledge formation, it
is important to understand the underlying mechanisms. In this seminar, I will show that sharing
memory engram cells underlies the linkage between memories (1), while synapse-specific plasticity
guarantees the identity and storage of individual memories (2). In addition, I will suggest that engram
cells in the hippocampus are organized into sub-ensembles representing distinct pieces of information,
which are then orchestrated to constitute an entire memory (3).
References
1. Yokose et al, Overlapping memory trace indispensable for linking, but not recalling, individualmemories. Science, 355: 398-403 (2017). doi:10.1126/science.aal2690
2. Abdou et al, Synapse-specific representation of the identity of overlapping memory engrams.
Science, 360: 1227-1231 (2018). doi:10.1126/science.aat3810
3. Ghandour et al, Orchestrated ensemble activities constitute a hippocampal memory engram.
Nature Communications, 10: 2637 (2019). doi:10.1038/s41467-019-10683-2

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Abstracts
Poster Presentation

P44

Synapse-specific plasticity governs the identity of overlapping
memory traces
K. Abdou, M. Shehata, K. Choko, H. Nishizono, M. Matsuo, S. Muramatsu, and K. InokuchiMemories are encoded and stored in specific neuronal ensemble, called engram cells. Some of thesememories are associated and stored in shared ensemble. However, brain machinery that underlies
memory storage and defines certain memory identity amidst numerous number of memories stored
in the same ensemble is poorly understood.
Here we show that when two associative memories are encoded in shared ensemble, engram-specificsynaptic plasticity delineates specific memory entity and that specific plasticity is both sufficient andcrucial for information storage. Using auditory fear conditioning and c-fos-TetTag system,
optogenetic stimulation of the activated ensemble terminals of auditory cortex (AC) and medial
geniculate nucleus (MGm) in lateral amygdala (LA) after complete retrograde amnesia -accomplishedby autophagy induction with protein synthesis inhibition- failed to induce memory recall at recent
and remote time points, indicating that memory engram no longer exists in that circuit. This result
was correlated with the resetting of plasticity and functional connectivity between the engram
assemblies. Furthermore, potentiating or depotentiating the plasticity at synapses specific to a given
memory did not affect the linked memory that is encoded in the same ensemble, suggesting thatmemories are stored in specific synapses.
These findings unravel how the brain organizes and stores multiple associative memories in sharedensemble, underpinning a causal relationship between synaptic input-specific plasticity and memory
identity and storage. Moreover, our study sheds light on the capability of selective and integral erasureof memory trace from the engram network, suggesting a potential way to treat post-traumatic stressdisorder (PTSD).

P45Manipulation of fear memory association by posterior parietal cortex
A. Suzuki, S. Kosugi, E. Murayama, N. Ohkawa, M. Matsuo,
H. Nishizono, and K. Inokuchi
The association of fear memory occurs when a conditioned stimulus (CS) is paired with an
unconditioned stimulus (US). Although previous studies suggested that some of brain regions
responded to CS and US signals, it is still unclear how the association regulates.
Here we show that the cellular ensemble in Posterior Parietal Cortex (PPC) specifically modulates
CS-US association without the processing of CS and US information. In the modified context-preexposure facilitation effect (CPFE) paradigm, optical silencing of PPC neurons which responded tocontext exposure (CS), when mice received footshock (US) in the same context, failed to associate
the context (CS) and the shock (US). On the other hand, optical activation of PPC neurons which
responded to context exposure, when mice received footshock in a different context, generated an
artificial CS-US associative memory, in which mice showed a freezing response in the initial context
where mice did not received footshock, but not in the neutral context. Furthermore, 15 min opticallysilencing of PPC neurons that responded during reactivation of CS-US associate memory that has
been once formed immediately after CS exposure 1 day after reactivation suppressed fear memory
when mice were tested 1 day later without optical silencing. Thus, manipulating the PPC activity
diassociate CS-US associative memory.

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