Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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RhoA-ROCK Inhibition Reverses Synaptic Remodeling and Motor and Cognitive Deficits Caused by Traumatic Brain Injury.Diminished dentate gyrus filtering of cortical input leads to enhanced area CA3 excitability after mild traumatic brain injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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Akiva S Cohen

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Kaitlin A Folweiler

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Rosalia Paterno

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P2860

Executive functions

What are the differences between long-term, short-term, and working memory?

Memory engram storage and retrieval

Animal models of traumatic brain injury

Morris water maze: procedures for assessing spatial and related forms of learning and memory

Developments of a water-maze procedure for studying spatial learning in the rat

Simple memory: a theory for archicortex

Environmental enrichment as a viable neurorehabilitation strategy for experimental traumatic brain injury.

A Multiscale Approach to Blast Neurotrauma Modeling: Part I - Development of Novel Test Devices for in vivo and in vitro Blast Injury Models

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10.1007/S11910-017-0762-X

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pathophysiology

traumatic brain injury

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Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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P2860

P2860

Pathophysiology and Treatment of Memory Dysfunction After Traumatic Brain Injury.

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