Korean J Anesthesiol.  2017 Jun;70(3):335-340. 10.4097/kjae.2017.70.3.335.

Apocynin preserves glutamatergic neurons in the basolateral amygdala in mice with neonatal sevoflurane exposure

• Sun Z
• Satomoto M
• Adachi YU
• Makita K

• KMID: 2382751
• DOI: http://doi.org/10.4097/kjae.2017.70.3.335

Abstract

BACKGROUND
Neonatal exposure to anesthetics induces neuronal apoptosis and long-term cognitive dysfunction in rodents. We showed that the nicotinamide adenine dinucleotide phosphate-oxidase inhibitor apocynin not only reduces neurotoxicity by decreasing superoxide levels and preventing mitochondrial dysfunction but also improves long-term memory impairment in neonatal mice exposed to sevoflurane. We also found that after the contextual fear conditioning test, glutamatergic neurons expressed c-Fos (neural activation) regardless of previous exposure to sevoflurane. Moreover, there were fewer c-Fos-expressing glutamatergic neurons in the basolateral amygdala (BLA) after exposure to sevoflurane than after exposure to carrier gas. In this study, we investigated whether the administration of apocynin prior to sevoflurane exposure would preserve glutamatergic neurons in the BLA.
METHODS
Apocynin (50 mg/kg) was injected intraperitoneally into six-day-old male mice 30 min before 6 h of exposure to 3% sevoflurane or carrier gas only. The mice were allowed to mature and then were subjected to the contextual fear conditioning test. The neural activation and neuron population in the BLA were investigated 2 h later.
RESULTS
Administration of apocynin prior to neonatal sevoflurane exposure not only prevented learning deficits but also preserved c-Fos-expressing glutamatergic neurons in the BLA.
CONCLUSIONS
Apocynin mitigates the cognitive impairment induced by neonatal sevoflurane exposure and preserves c-Fos-expressing glutamatergic neurons in the basolateral amygdala.

Keyword

Anesthesia; Brain; Neurotoxicity; Pediatrics; Sevoflurane

MeSH Terms

Anesthesia
Anesthetics
Animals
Apoptosis
Basolateral Nuclear Complex*
Brain
Cognition Disorders
Humans
Learning
Male
Memory, Long-Term
Mice*
NAD
Neurons*
Pediatrics
Rodentia
Superoxides
Anesthetics
NAD
Superoxides