Inhibition of NADPH oxidase 2 (NOX2) reverses cognitive deficits by modulating excitability and excitatory transmission in the hippocampus after traumatic brain injury.
Biochem Biophys Res Commun
; 617(Pt 1): 1-7, 2022 08 20.
Article
em En
| MEDLINE
| ID: mdl-35660876
ABSTRACT
Traumatic brain injury (TBI) is a closed or open head injury caused by external mechanical forces that induce brain damage, resulting in a wide range of postinjury dysfunctions of emotions, learning and memory, adversely affecting the quality of life of patients. In this study, we aimed to explore the possible mechanisms of NOX2 on cognitive deficits in a TBI mouse model. Behavioral tests were applied to evaluate learning and memory ability, and electrophysiological experiments were performed to measure synaptic transmission and intrinsic excitability of the CA1 pyramidal cells (PCs) and long-term potentiation (LTP) in the TBI hippocampus. We found that inhibitors of nicotinamide adenine dinucleotide phosphate oxidase 2 (NADPH oxidase 2; NOX2) (GSK2795039 and apocynin) attenuate neurological deficits, facilitate long-term potentiation (LTP) and decrease spontaneous synaptic transmission and intrinsic excitability of CA1 pyramidal cells (PCs) in traumatic brain injury (TBI) mice. NOX2-/- mice display reduced learning and memory impairment, enhanced LTP and reduced spontaneous synaptic transmission and intrinsic excitability of PCs after TBI. Our study demonstrates that NOX2 is a potential target for learning and memory by modulating excitability and excitatory transmission in the hippocampus after TBI.
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Base de dados:
MEDLINE
Assunto principal:
Qualidade de Vida
/
Lesões Encefálicas Traumáticas
Limite:
Animals
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Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2022
Tipo de documento:
Article