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Carol A. Barnes

Researcher at University of Arizona

Publications -  277
Citations -  40601

Carol A. Barnes is an academic researcher from University of Arizona. The author has contributed to research in topics: Hippocampal formation & Hippocampus. The author has an hindex of 98, co-authored 272 publications receiving 37781 citations. Previous affiliations of Carol A. Barnes include University of Oslo & University of California, Davis.

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NMDA receptor antagonism blocks experience-dependent expansion of hippocampal "place fields".

TL;DR: The effects of CPP mimic changes that occur during normal aging, suggesting mechanisms by which sequence learning deficits may arise in aged animals.
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Spatial exploration induces ARC, a plasticity-related immediate-early gene, only in calcium/calmodulin-dependent protein kinase II-positive principal excitatory and inhibitory neurons of the rat forebrain.

TL;DR: The data reported here show that behavior‐ or seizure‐induced Arc expression in the hippocampus, primary somatosensory cortex, and dorsal striatum of rats colocalizes only with neuronal (NeuN‐positive) and not with glial (GFAP‐ positive) cells, consistent with the hypothesis that Arc and CaMKII act as plasticity partners to promote functional and/or structural synaptic modifications that accompany learning.
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Spatial representation along the proximodistal axis of CA1

TL;DR: The findings suggest that spatial firing in CA1 is organized transversally, with the strongest spatial modulation occurring in the MEC-associated proximal part.
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The Aging Navigational System.

TL;DR: This review discusses emerging evidence from rodents, non-human primates, and humans that demonstrates how cognitive aging affects the navigational computations supported by neuronal systems and the clinical potential of behavioral and neural markers of spatial navigation, with a particular emphasis on neurodegenerative disorders.
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Self-Motion and the Hippocampal Spatial Metric

TL;DR: The spatial scale over which the hippocampal population vector is updated appears to be derived primarily from the gain of a self-motion velocity signal with approximately equal components derived from ambulation, vestibular, and optic-flow signals.