What does the anatomical organization of the entorhinal cortex tell us
TLDR
In this article, the authors argue that layers in entorhinal cortex show different functional characteristics most likely not on the basis of strikingly different inputs or outputs, but much more likely due to differences in intrinsic organization, combined with very specific sets of inputs.Abstract:
The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. The finding of the grid cells in all layers and reports on interactions between deep and superficial layers indicate that this rather simplistic perception may be at fault. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that layers in entorhinal cortex show different functional characteristics most likely not on the basis of strikingly different inputs or outputs, but much more likely on the basis of differences in intrinsic organization, combined with very specific sets of inputs. Here, we aim to summarize recent anatomical data supporting the notion that the traditional description of the entorhinal cortex as a layered input-output structure for the hippocampal formation does not give the deserved credit to what this structure might be contributing to the overall functions of cortico-hippocampal networks.read more
Citations
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Functional organization of the hippocampal longitudinal axis
TL;DR: Together, anatomical studies and electrophysiological recordings in rodents suggest a model in which functional long-axis gradients are superimposed on discrete functional domains, which provides a potential framework to explain and test the multiple functions ascribed to the hippocampus.
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Propagation of Tau Pathology in a Model of Early Alzheimer’s Disease
Alix de Calignon,Manuela Polydoro,Marc Suárez-Calvet,Marc Suárez-Calvet,Christopher William,David H. Adamowicz,Katherine J. Kopeikina,Katherine J. Kopeikina,Rose Pitstick,Naruhiko Sahara,Karen H. Ashe,George A. Carlson,Tara L. Spires-Jones,Bradley T. Hyman +13 more
TL;DR: A transgenic mouse model in which overexpression of human tau P301L is restricted to EC-II is described, suggesting that a sequence of progressive misfolding of tau proteins, circuit-based transfer to new cell populations, and deafferentation induced degeneration are part of a process of t Tau-induced neurodegeneration.
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Hippocampal Replay of Extended Experience
TL;DR: It is shown, using a neural decoding approach, that firing sequences corresponding to long runs through a large environment are replayed with high fidelity and that such replay can begin at remote locations on the track, which suggests that extended replay is composed of chains of shorter subsequences.
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Hippocampal GABAergic Inhibitory Interneurons.
Kenneth A. Pelkey,Ramesh Chittajallu,Michael T. Craig,Ludovic Tricoire,Ludovic Tricoire,Jason C. Wester,Jason C. Wester,Chris J. McBain,Chris J. McBain +8 more
TL;DR: An overview of the current state of the field of interneuron research, focusing largely on the hippocampus, discusses recent advances related to the various cell types, including their development and maturation, expression of subtype-specific voltage- and ligand-gated channels, and their roles in network oscillations.
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Molecular drivers and cortical spread of lateral entorhinal cortex dysfunction in preclinical Alzheimer's disease
Usman A. Khan,Li Liu,Frank A. Provenzano,Diego E. Berman,Caterina P. Profaci,Richard P. Sloan,Richard Mayeux,Karen Duff,Scott A. Small +8 more
TL;DR: The fMRI variant used to address basic questions about entorhinal cortex pathophysiology found that the LEC was affected in preclinical disease, that LEC dysfunction could spread to the parietal cortex duringPreclinical disease and that APP expression potentiated tau toxicity in driving L EC dysfunction, thereby helping to explain regional vulnerability in the disease.
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