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Juan Carlos Tapia

Researcher at Harvard University

Publications -  24
Citations -  2530

Juan Carlos Tapia is an academic researcher from Harvard University. The author has contributed to research in topics: Neuromuscular junction & Medicine. The author has an hindex of 14, co-authored 19 publications receiving 2199 citations. Previous affiliations of Juan Carlos Tapia include Washington University in St. Louis.

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Saturated Reconstruction of a Volume of Neocortex

TL;DR: In this paper, the authors describe automated technologies to probe the structure of neural tissue at nanometer resolution and use them to generate a saturated reconstruction of a sub-volume of mouse neocortex in which all cellular objects (axons, dendrites, and glia) and many subcellular components (synapses, synaptic vesicles, spines, spine apparati, postsynaptic densities, and mitochondria) are rendered and itemized in a database.
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High-contrast en bloc staining of neuronal tissue for field emission scanning electron microscopy

TL;DR: This technique uses osmium impregnation (OTO) to make the samples conductive while heavily staining membranes for segmentation studies to produce clean, highly contrasted TEM and scanning electron microscopy (SEM) samples of insect, fish and mammalian nervous systems.
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Gamma protocadherins are required for synaptic development in the spinal cord

TL;DR: Evidence is provided for a direct role of gamma-Pcdhs in synaptic development and genetic tools for elucidating their contribution to synaptic specificity are established.
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Shared Resistance to Aging and ALS in Neuromuscular Junctions of Specific Muscles

TL;DR: Analysis of skeletal neuromuscular junctions in mice reveals novel structural, regional and molecular parallels between aging and ALS and finds that muscles respond in one of three ways to aging.
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Lethal impairment of cholinergic neurotransmission in hemicholinium-3-sensitive choline transporter knockout mice.

TL;DR: It is demonstrated that CHT is an essential and regulated presynaptic component of cholinergic signaling and indicates that it warrants consideration as a candidate gene for disorders characterized byCholinergic hypofunction.