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Masaki Hiramoto

Researcher at Scripps Research Institute

Publications -  9
Citations -  143

Masaki Hiramoto is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Retina & Retinal ganglion. The author has an hindex of 4, co-authored 9 publications receiving 108 citations.

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Convergence of multisensory inputs in Xenopus tadpole tectum.

TL;DR: The layer‐specific projections of the hindbrain and retinal axons suggest a functional segregation of sensory inputs to proximal and distal tectal cell dendrites, respectively.
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An Evolutionarily Conserved Mechanism for Activity-Dependent Visual Circuit Development

TL;DR: The idea that retinal waves in amniotes, the animals that develop either in ovo or utero (namely reptiles, birds and mammals) could be an evolutionary adaptation to life on land is contemplated, and it is predicted that the experience-dependent development of the tadpole visual system is a blueprint of what will be found in future studies of the effects of spontaneousretinal waves on instructing development of retinorecipient targets.
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Optic flow instructs retinotopic map formation through a spatial to temporal to spatial transformation of visual information

TL;DR: It is demonstrated that a spatial to temporal to spatial transformation of visual information controls experience-dependent topographic map plasticity, and is likely to apply to other sensory modalities and projections in the brain.
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Experience-Dependent Bimodal Plasticity of Inhibitory Neurons in Early Development.

TL;DR: It is found that developing inhibitory neurons fall into distinct functional groups with opposite experience-dependent plasticity and as such, are well positioned to foster experience- dependent synaptic Plasticity and maintain circuit stability during labile periods of circuit development.
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Dctn1 binds to tdp-43 and regulates tdp-43 aggregation

TL;DR: In this paper, the authors used a panel of truncated mutants to identify a new player in TDP-43 cytoplasmic-nuclear transport, and showed that dysregulation of DCTN1-TDP43 interactions triggers mislocalization and aggregation of TDP43, thus providing insights into the pathological mechanisms of Perry disease.