Sevoflurane induced amnesia inhibits hippocampal Arc expression partially through 5-hydroxytryptamine-7 receptors in the bilateral basolateral amygdala in rats

•Sevoflurane could induce amnesia and inhibit hippocampal Arc expression after fear conditioning.•The effects could be reversed by BLA infusion of SB269970 and exacerbated by AS-19.•Sevoflurane might not induce neuroapoptosis in the hippocampus.

This study aimed to investigate whether the regulation of 5-hydroxytryptamine-7 (5-HT7) receptors in the bilateral basolateral amygdala (BLA) could alter the amnesic effects of sevoflurane and change the hippocampal expression of Arc and neural apoptosis. Male Sprague-Dawley rats were randomized into ten groups. First, the animals received bilateral injection of SB269970 (20, 50, or 100 pmol/0.2 μl) or saline (0.2 μl) or AS-19 (2, 10, or 50 pmol/0.2 μl), followed by inhalation of 2% sevoflurane or air for 2 h. Then, fear conditioning training was carried out, and the percentage of freezing was detected 24 h later. Furthermore, hippocampal Arc protein level and neural apoptosis were measured. Pre-training inhalation of sevoflurane reduced the extent of freezing, and hippocampal Arc expression. The largest dose of SB269970 (100 pmol) could block sevoflurane-induced amnesia and reverse the inhibitive effect of sevoflurane on Arc expression, while the maximal dose of AS-19 could exacerbate the amnesic effect, and further inhibit Arc expression. Furthermore, pre-training inhalation of 2% sevoflurane for 6 h could not induce neural apoptosis in the hippocampus. The amnesic effect of sevoflurane might partly attribute to its impairment of memory formation in the hippocampus via activation of 5-HT7 receptors in the BLA.