Research Article
No access
Published Online: 25 July 2006

Enhanced Catecholamine Synthesis in the Prefrontal Cortex after Traumatic Brain Injury: Implications for Prefrontal Dysfunction

Publication: Journal of Neurotrauma
Volume 23, Issue Number 7

Abstract

Traumatic brain injury (TBI)–induced dysfunction of the prefrontal cortex causes many high-level cognitive deficits, including working memory (WM) dysfunction. WM lies at the core of many highlevel functions, yet the cellular and molecular mechanisms underlying its dysfunction are poorly understood. Lesion and pharmacological studies in rodents have implicated the medial prefrontal cortex (mPFC), which includes the prelimbic/infralimbic (PL/IL) cortices, in WM tasks. These studies have shown that optimal levels of catecholamine neurotransmission are critical for normalcy of WM function, suggesting that alterations in their synthesis may play a role in WM dysfunction. Using the cortical impact injury model of traumatic brain injury which reproducibly causes working memory deficits in rodents, we have measured the protein levels and activity of tyrosine hydroxylase (TH), the rate-limiting enzyme for catecholamine biosynthesis, and tissue dopamine (DA) and norepinephrine (NE) levels in microdissected PL/IL tissues. Our results show that TBI increases TH protein levels, its activity and tissue DA and NE content in the PL/IL. These findings suggest that altered catecholamine signaling within the PL/IL may contribute to impaired PFC function, and may have implications in the design and implementation of strategies to alleviate prefrontal dysfunction in brain injury patients.

Get full access to this article

View all available purchase options and get full access to this article.

Information & Authors

Information

Published In

cover image Journal of Neurotrauma
Journal of Neurotrauma
Volume 23Issue Number 7July 2006
Pages: 1094 - 1102
PubMed: 16866622

History

Published online: 25 July 2006
Published in print: July 2006

Permissions

Request permissions for this article.

Topics

Authors

Affiliations

Nobuhide Kobori
Vivian L. Smith Center for Neurological Research, Department of Neurobiology and Anatomy, and Department of Neurosurgery, University of Texas Medical School at Houston, Houston Texas.
Guy L. Clifton
Vivian L. Smith Center for Neurological Research, Department of Neurobiology and Anatomy, and Department of Neurosurgery, University of Texas Medical School at Houston, Houston Texas.
Pramod K. Dash
Vivian L. Smith Center for Neurological Research, Department of Neurobiology and Anatomy, and Department of Neurosurgery, University of Texas Medical School at Houston, Houston Texas.

Metrics & Citations

Metrics

Citations

Export citation

Select the format you want to export the citations of this publication.

View Options

Access content

To read the fulltext, please use one of the options below to sign in or purchase access.

Society Access

If you are a member of a society that has access to this content please log in via your society website and then return to this publication.

Restore your content access

Enter your email address to restore your content access:

Note: This functionality works only for purchases done as a guest. If you already have an account, log in to access the content to which you are entitled.

View options

PDF/EPUB

View PDF/EPUB

Figures

Tables

Media

Share

Share

Copy the content Link

Share on social media

Back to Top