Traumatic Brain Injury Upregulates Phosphodiesterase Expression in the Hippocampus

Frontiers in Systems Neuroscience
Nicole M WilsonColeen M Atkins

Abstract

Traumatic brain injury (TBI) results in significant impairments in hippocampal synaptic plasticity. A molecule critically involved in hippocampal synaptic plasticity, 3',5'-cyclic adenosine monophosphate, is downregulated in the hippocampus after TBI, but the mechanism that underlies this decrease is unknown. To address this question, we determined whether phosphodiesterase (PDE) expression in the hippocampus is altered by TBI. Young adult male Sprague Dawley rats received sham surgery or moderate parasagittal fluid-percussion brain injury. Animals were analyzed by western blotting for changes in PDE expression levels in the hippocampus. We found that PDE1A levels were significantly increased at 30 min, 1 h and 6 h after TBI. PDE4B2 and 4D2 were also significantly increased at 1, 6, and 24 h after TBI. Additionally, phosphorylation of PDE4A was significantly increased at 6 and 24 h after TBI. No significant changes were observed in levels of PDE1B, 1C, 3A, 8A, or 8B between 30 min to 7 days after TBI. To determine the spatial profile of these increases, we used immunohistochemistry and flow cytometry at 24 h after TBI. PDE1A and phospho-PDE4A localized to neuronal cell bodies. PDE4B2 was expressed in neuronal dendrites, microgl...Continue Reading

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Citations

May 18, 2017·Neural Plasticity·Michael J HylinRyan Holden
Nov 11, 2019·Trends in Pharmacological Sciences·Arjan BloklandJos Prickaerts
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Methods Mentioned

BETA
flow cytometry

Software Mentioned

GraphPad Prism
Kaluza
ImageJ
pClamp
SigmaPlot

Related Concepts

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Brain Injury & Trauma

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