Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior
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Author
Beitchman, Joshua AGriffiths, Daniel R
Hur, Yerin
Ogle, Sarah B
Bromberg, Caitlin E
Morrison, Helena W
Lifshitz, Jonathan
Adelson, P David
Thomas, Theresa Currier
Affiliation
Univ Arizona, Dept Child Hlth, Coll Med PhoenixUniv Arizona, Coll Nursing
Issue Date
2020-01-21
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FRONTIERS MEDIA SACitation
Beitchman JA, Griffiths DR, Hur Y, Ogle SB, Bromberg CE, Morrison HW, Lifshitz J, Adelson PD and Currier Thomas T (2020) Experimental Traumatic Brain Injury Induces Chronic Glutamatergic Dysfunction in Amygdala Circuitry Known to Regulate Anxiety-Like Behavior. Front. Neurosci. 13:1434. doi: 10.3389/fnins.2019.01434Journal
FRONTIERS IN NEUROSCIENCERights
Copyright © 2020 Beitchman, Griffiths, Hur, Ogle, Bromberg, Morrison, Lifshitz, Adelson and Currier Thomas. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Up to 50% of traumatic brain injury (TBI) survivors demonstrate persisting and late-onset anxiety disorders indicative of limbic system dysregulation, yet the pathophysiology underlying the symptoms is unclear. We hypothesize that the development of TBI-induced anxiety-like behavior in an experimental model of TBI is mediated by changes in glutamate neurotransmission within the amygdala. Adult, male Sprague-Dawley rats underwent midline fluid percussion injury or sham surgery. Anxiety-like behavior was assessed at 7 and 28 days post-injury (DPI) followed by assessment of real-time glutamate neurotransmission in the basolateral amygdala (BLA) and central nucleus of the amygdala (CeA) using glutamate-selective microelectrode arrays. The expression of anxiety-like behavior at 28 DPI coincided with decreased evoked glutamate release and slower glutamate clearance in the CeA, not BLA. Numerous factors contribute to the changes in glutamate neurotransmission over time. In two additional animal cohorts, protein levels of glutamatergic transporters (Glt-1 and GLAST) and presynaptic modulators of glutamate release (mGluR2, TrkB, BDNF, and glucocorticoid receptors) were quantified using automated capillary western techniques at 28 DPI. Astrocytosis and microglial activation have been shown to drive maladaptive glutamate signaling and were histologically assessed over 28 DPI. Alterations in glutamate neurotransmission could not be explained by changes in protein levels for glutamate transporters, mGluR2 receptors, astrocytosis, and microglial activation. Presynaptic modulators, BDNF and TrkB, were significantly decreased at 28 DPI in the amygdala. Dysfunction in presynaptic regulation of glutamate neurotransmission may contribute to anxiety-related behavior and serve as a therapeutic target to improve circuit function.Note
Open access journalISSN
1662-453XPubMed ID
32038140Version
Final published versionae974a485f413a2113503eed53cd6c53
10.3389/fnins.2019.01434
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Except where otherwise noted, this item's license is described as Copyright © 2020 Beitchman, Griffiths, Hur, Ogle, Bromberg, Morrison, Lifshitz, Adelson and Currier Thomas. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).
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