scispace - formally typeset
D

Donald C. Lo

Researcher at Duke University

Publications -  95
Citations -  9804

Donald C. Lo is an academic researcher from Duke University. The author has contributed to research in topics: Huntingtin & Neuroprotection. The author has an hindex of 41, co-authored 93 publications receiving 8925 citations. Previous affiliations of Donald C. Lo include Medical Park & Wake Forest University.

Papers
More filters
Journal ArticleDOI

Neurotrophins and synaptic plasticity.

TL;DR: The evidence implicating neurotrophins as molecular mediators of synaptic and morphological plasticity, and the rules and mechanisms by which they exert their effects remain intriguingly elusive are discussed.
Journal ArticleDOI

Neurotrophins regulate dendritic growth in developing visual cortex

TL;DR: The spectrum of neurotrophic actions and the laminar specificity of these actions implicate endogenous neurotrophins as regulatory signals in the development of specific dendritic patterns in mammalian neocortex.
Journal ArticleDOI

Ferrostatins inhibit oxidative lipid damage and cell death in diverse disease models.

TL;DR: A mechanistic model to explain the activity of Fer-1 was developed, which guided the development of ferrostatins with improved properties, and that lipid peroxidation mediates diverse disease phenotypes are suggested.
Journal ArticleDOI

Opposing roles for endogenous BDNF and NT-3 in regulating cortical dendritic growth.

TL;DR: These antagonistic actions of endogenous BDNF and NT-3 provide a mechanism by which dendritic growth and retraction can be dynamically regulated during cortical development, and suggest that the multiple neurotrophins expressed in developing cortex represent distinct components of an extracellular signaling system for regulating dendrite growth.
Journal ArticleDOI

Neurotrophin regulation of cortical dendritic growth requires activity

TL;DR: In ferret cortical brain slices, the interactions between activity and neurotrophins in regulating dendritic growth of layer 4 pyramidal neurons were examined, finding that inhibition of spontaneous electrical activity, synaptic transmission, or L-type calcium channels each prevented the otherwise dramatic increase in dendrite arborizations elicited by brain-derived neurotrophic factor.