scispace - formally typeset
M

Motojiro Yoshihara

Researcher at National Institute of Information and Communications Technology

Publications -  12
Citations -  1504

Motojiro Yoshihara is an academic researcher from National Institute of Information and Communications Technology. The author has contributed to research in topics: Synaptotagmin 1 & Vesicle fusion. The author has an hindex of 10, co-authored 12 publications receiving 1414 citations. Previous affiliations of Motojiro Yoshihara include Picower Institute for Learning and Memory & Massachusetts Institute of Technology.

Papers
More filters
Journal ArticleDOI

Cytoplasmic aggregates trap polyglutamine-containing proteins and block axonal transport in a Drosophila model of Huntington's disease.

TL;DR: These findings indicate that nonnuclear events induced by cytoplasmic huntingtin aggregation play a central role in the progressive neurodegeneration observed in Huntington's disease.
Journal ArticleDOI

Synaptotagmin I Functions as a Calcium Sensor to Synchronize Neurotransmitter Release

TL;DR: The data suggest the Ca(2+) cooperativity of neurotransmitter release is likely mediated through synaptotagmin-SNARE interactions, while phospholipid binding and oligomerization trigger rapid fusion with increased release probability.
Journal ArticleDOI

Retrograde Signaling by Syt 4 Induces Presynaptic Release and Synapse-Specific Growth

TL;DR: It is demonstrated that postsynaptic calcium 2+ ion (Ca2+) influx through glutamate receptors and subsequent post synapse vesicle fusion trigger a robust induction of presynaptic miniature release after high-frequency stimulation at Drosophila neuromuscular junctions.
Journal ArticleDOI

Presynaptic N-type Calcium Channels Regulate Synaptic Growth

TL;DR: It is reported that presynaptic N-type calcium channels not only control neurotransmitter release but also regulate synaptic growth at Drosophila neuromuscular junctions, and linking presynptic voltage-gated calcium entry to downstream calcium-sensitive synaptic growth regulators provides an efficient activity-dependent mechanism for modifying synaptic strength.