Sevoflurane-induced cognitive effect on α7-nicotine receptor and M1 acetylcholine receptor expression in the hippocampus of aged rats.

Abstract

Background: Sevoflurane treatment increases the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD show a decline in cognitive abilities compared to preoperative levels.

Objectives: This study aimed to investigate whether the activation of α7 nicotinic acetylcholine receptor (α7nAChR) and the expression of M₁ acetylcholine receptor (mAChR M₁) in the hippocampus affects the cognitive function of aged rats.

Methods: Forty-eight Sprague-Dawley (SD) rats of 1-week- and 12-months-old were divided into eight groups: four groups for α7nAChR and four groups for mAChR M₁, respectively. All SD rats received 1.0-02% sevoflurane for α7nAChR and 1.0-02% sevoflurane for mAChR M₁ for 2-6 h, respectively. The Y-maze test was used to assess the ability to learn and memory after receiving sevoflurane for 7 days at the same moment portion. RT-PCR was used to determine the expression of α7nAChR and mAChR M₁ in the hippocampus of rats.

Results: The α7nAChR mitigated the formation of sevoflurane-induced memory impairment by modulating the translocation of NR2B from the intracellular reservoir to the cell surface reservoir within the hippocampus. Next, sevoflurane-induced decline of cognitive function and significantly decreased mAChR M₁ expression at mRNA levels.

Conclusion: α7nAChR regulates the trafficking of NR2B in the hippocampus of rats via the Src-family tyrosine kinase (SFK) pathway. This regulation is associated with cognitive deficits induced by sevoflurane in hippocampal development. Sevoflurane affects the cognitive function of rats by suppressing the mAChR M₁ expression at mRNA levels in the hippocampus.