scispace - formally typeset
B

Bruce S. McEwen

Researcher at Rockefeller University

Publications -  1168
Citations -  214913

Bruce S. McEwen is an academic researcher from Rockefeller University. The author has contributed to research in topics: Hippocampus & Hippocampal formation. The author has an hindex of 215, co-authored 1163 publications receiving 200638 citations. Previous affiliations of Bruce S. McEwen include Yale University & National Institutes of Health.

Papers
More filters
Journal ArticleDOI

Rat Brain Binds Adrenal Steroid Hormone: Radioautography of Hippocampus with Corticosterone

TL;DR: The nuclei of many neurons were clearly labeled but radioactivity was relatively sparse in the cytoplasm, in the axons where they branch from cell bodies, and in adjacent neuropil.
Journal ArticleDOI

Stress, sex, and neural adaptation to a changing environment: mechanisms of neuronal remodeling.

TL;DR: This review will illustrate the actions of estrogen on synapse formation in the hippocampus and the process of stress‐induced remodeling of dendrites and synapses in the hippocamp, amygdala, and prefrontal cortex.
Journal ArticleDOI

Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

TL;DR: It is found that 12- to 15-month-old Tg2576 mice lacking the catalytic subunit Nox2 of NADPH oxidase do not develop oxidative stress, cerebrovascular dysfunction, or behavioral deficits, and improvements occurred without reductions in brain amyloid-β peptide levels or amyloids plaques.
Journal ArticleDOI

Tracking the estrogen receptor in neurons: Implications for estrogen-induced synapse formation

TL;DR: Findings support a testable model in which local, non-genomic regulation by estrogen participates along with genomic actions of estrogens in the regulation of synapse formation, and a more local role for E in CA1 neurons seems likely.
Journal ArticleDOI

Structural and functional alterations to rat medial prefrontal cortex following chronic restraint stress and recovery.

TL;DR: The hypothesis that disease-related PFC dysfunction is a consequence of network disruption secondary to altered structural and functional plasticity and that circuitry reestablishment may underlie elements of recovery is supported.