Ceftriaxone Treatment Preserves Cortical Inhibitory Interneuron Function via Transient Salvage of GLT-1 in a Rat Traumatic Brain Injury Model.
Animals
Anti-Bacterial Agents
/ administration & dosage
Brain Injuries, Traumatic
/ metabolism
Ceftriaxone
/ administration & dosage
Disease Models, Animal
Excitatory Amino Acid Transporter 2
/ metabolism
GABAergic Neurons
/ metabolism
Gene Expression
Interneurons
/ metabolism
Male
Motor Cortex
/ physiopathology
Parvalbumins
/ metabolism
Rats, Sprague-Dawley
GLT-1
ceftriaxone
intracortical inhibition
parvalbumin
traumatic brain injury
Journal
Cerebral cortex (New York, N.Y. : 1991)
ISSN: 1460-2199
Titre abrégé: Cereb Cortex
Pays: United States
ID NLM: 9110718
Informations de publication
Date de publication:
17 12 2019
17 12 2019
Historique:
received:
07
09
2018
revised:
26
11
2018
accepted:
28
11
2018
pubmed:
28
12
2018
medline:
21
10
2020
entrez:
28
12
2018
Statut:
ppublish
Résumé
Traumatic brain injury (TBI) results in a decrease in glutamate transporter-1 (GLT-1) expression, the major mechanism for glutamate removal from synapses. Coupled with an increase in glutamate release from dead and dying neurons, this causes an increase in extracellular glutamate. The ensuing glutamate excitotoxicity disproportionately damages vulnerable GABAergic parvalbumin-positive inhibitory interneurons, resulting in a progressively worsening cortical excitatory:inhibitory imbalance due to a loss of GABAergic inhibitory tone, as evidenced by chronic post-traumatic symptoms such as epilepsy, and supported by neuropathologic findings. This loss of intracortical inhibition can be measured and followed noninvasively using long-interval paired-pulse transcranial magnetic stimulation with mechanomyography (LI-ppTMS-MMG). Ceftriaxone, a β-lactam antibiotic, is a potent stimulator of the expression of rodent GLT-1 and would presumably decrease excitotoxic damage to GABAergic interneurons. It may thus be a viable antiepileptogenic intervention. Using a rat fluid percussion injury TBI model, we utilized LI-ppTMS-MMG, quantitative PCR, and immunohistochemistry to test whether ceftriaxone treatment preserves intracortical inhibition and cortical parvalbumin-positive inhibitory interneuron function after TBI in rat motor cortex. We show that neocortical GLT-1 gene and protein expression are significantly reduced 1 week after TBI, and this transient loss is mitigated by ceftriaxone. Importantly, whereas intracortical inhibition declines progressively after TBI, 1 week of post-TBI ceftriaxone treatment attenuates the loss of inhibition compared to saline-treated controls. This finding is accompanied by significantly higher parvalbumin gene and protein expression in ceftriaxone-treated injured rats. Our results highlight prospects for ceftriaxone as an intervention after TBI to prevent cortical inhibitory interneuron dysfunction, partly by preserving GLT-1 expression.
Identifiants
pubmed: 30590449
pii: 5257442
doi: 10.1093/cercor/bhy328
pmc: PMC7150617
doi:
Substances chimiques
Anti-Bacterial Agents
0
Excitatory Amino Acid Transporter 2
0
Parvalbumins
0
Slc1a2 protein, rat
0
Ceftriaxone
75J73V1629
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4506-4518Subventions
Organisme : NINDS NIH HHS
ID : R01 NS088583
Pays : United States
Informations de copyright
© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
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