Metabotropic Glutamate Receptor 2 Expression Is Chronically Elevated in Male Rats With Post-Traumatic Stress Disorder Related Behavioral Traits Following Repetitive Low-Level Blast Exposure

De Gasperi, Rita; Gama Sosa, Miguel A.; Perez Garcia, Georgina; Perez, Gissel M.; Pryor, Dylan; Morrison, Chenel L-A.; Lind, Rachel; Abutarboush, Rania; Kawoos, Usmah; Statz, Jonathan K.; Patterson, Jacob; Hof, Patrick R.; Zhu, Carolyn W.; Ahlers, Stephen T.; Cook, David G.; Elder, Gregory A.

doi:10.1089/neu.2023.0252

Cited by 1 publication

(3 citation statements)

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“…mGluR2 is elevated after blast exposure in a time course that correlates with the appearance of the behavioral phenotype [27,301]. A causative role for mGluR2 elevation is supported by the prevention [28] or reversal [301] of the behavioral phenotype by mGluR2/3 antagonists. It is also supported by (2R, 6R) hydroxynorketamine's rescue of the phenotype [39] since (2R, 6R) hydroxynorketamine acts principally through mGluR2-related mechanisms [302,303].…”

Section: Neuronal Mglu2mentioning

confidence: 98%

“…While the neurobiological basis for the behavioral traits in our model are not fully understood, our most recent work suggests that the late behavioral traits seem to be caused by abnormalities in the group II metabotropic receptor mGluR2 [301]. mGluR2 is elevated after blast exposure in a time course that correlates with the appearance of the behavioral phenotype [27,301].…”

Section: Neuronal Mglu2mentioning

confidence: 98%

“…Finally, a proximate cause for the late neurobehavioral abnormalities seems to lie in the elevated expression of the group II metabotropic receptor mGluR2 [301]. However, the molecular basis for why mGluR2 elevation occurs and its relationship to an early vascular insult are unclear.…”

Section: Future Studiesmentioning

confidence: 99%

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The Neurovascular Unit as a Locus of Injury in Low-Level Blast-Induced Neurotrauma

Elder,

Gama Sosa,

De Gasperi

et al. 2024

IJMS

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Blast-induced neurotrauma has received much attention over the past decade. Vascular injury occurs early following blast exposure. Indeed, in animal models that approximate human mild traumatic brain injury or subclinical blast exposure, vascular pathology can occur in the presence of a normal neuropil, suggesting that the vasculature is particularly vulnerable. Brain endothelial cells and their supporting glial and neuronal elements constitute a neurovascular unit (NVU). Blast injury disrupts gliovascular and neurovascular connections in addition to damaging endothelial cells, basal laminae, smooth muscle cells, and pericytes as well as causing extracellular matrix reorganization. Perivascular pathology becomes associated with phospho-tau accumulation and chronic perivascular inflammation. Disruption of the NVU should impact activity-dependent regulation of cerebral blood flow, blood–brain barrier permeability, and glymphatic flow. Here, we review work in an animal model of low-level blast injury that we have been studying for over a decade. We review work supporting the NVU as a locus of low-level blast injury. We integrate our findings with those from other laboratories studying similar models that collectively suggest that damage to astrocytes and other perivascular cells as well as chronic immune activation play a role in the persistent neurobehavioral changes that follow blast injury.

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