The effect of sevoflurane on the expression of M1 acetylcholine receptor in the hippocampus and cognitive function of aged rats

Abstract

Our aim is to investigate the effect of 1.5 and 3.0% sevoflurane on the expression of M(1) acetylcholine receptor (mAChR M(1)) in the hippocampus and the cognitive function of aged rats. Forty Sprague-Dawley (SD) rats of 12-month old were randomly divided into five groups. All SD rats received 1.5 or 3.0% sevoflurane in a special glass anesthesia box for 2 h, respectively, except for the normal control group. Y-maze was used to test the ability of learning and memory after being received sevoflurane for 1 or 7 days at the same moment portion. The expression of mAChR M(1) in the hippocampus of rats was tested by RT-PCR. The results showed that 3% sevoflurane induced the decline of cognitive function and significantly decreased the mAChR M(1) expression at mRNA levels at 1 day in the 3.0% sevoflurane I group when compared with the normal control group. However, there was no significant difference among the other groups when compared with normal control group. Therefore, administration of sevoflurane might temporally affect the ability of cognitive function of rats through suppressing the mAChR M(1) expression at mRNA levels in hippocampus.

Isoflurane Reversibly Destabilizes Hippocampal Dendritic Spines by an Actin-Dependent Mechanism

“…General anesthetics potently block hippocampus-dependent memory formation and consolidation, both acutely [14], [15] and chronically [16]–[18], and following exposure during critical periods of neurodevelopment [19], [20]. Hippocampal long-term potentiation (LTP), a neurophysiological correlate of memory, is also blocked by anesthetics [16], [21].…”

Insecticide imidacloprid influences cognitive functions and alters learning performance and related gene expression in a rat model

“…; Peng et al . ). The effects of IMI on some genes related to cognitive function and learning especially in subchronic period are not fully known.…”

Positive Allosteric Modulation of the Muscarinic M1Receptor Improves Efficacy of Antipsychotics in Mouse Glutamatergic Deficit Models of Behavior

“…In contrast with the PPI studies, the atypical antipsychotics, clozapine and aripiprazole, but not haloperidol, showed an enhancement of efficacy by BQCA in reversing MK-801-induced spatial memory disruption in the Y-maze. The hippocampus has a high expression of M 1 mAChRs, which are important for memory formation in rodents (Talts et al, 1998;Anagnostaras et al, 2003;Lee and Kesner, 2003;Newell et al, 2007;Mauck et al, 2010;Peng et al, 2012). Indeed, BQCA enhances baseline spatial and object recognition memory in rodents (Chambon et al, 2011(Chambon et al, , 2012, reverses scopolamine-disrupted fear and working memory, and restores memory function in Tg2576 mice (Ma et al, 2009;Shirey et al, 2009;Chambon et al, 2012).…”

“…In terms of the brain regions mediating the interactions between the M 1 mAChR PAM and antipsychotics in our models, it is likely that cortical and striatal regions are involved in the PPI effects, since they express the M 1 mAChR (Han et al, 2008;Ma et al, 2009;Peng et al, 2012) and have been implicated in regulation of sensorimotor gating mechanisms (Swerdlow et al, 1990Geyer et al, 2001;Braff, 2010). Although the M 1 mAChR is also found in the hippocampus, it is unlikely to be as important in the observed effects, as MK-801-induced PPI disruption does not involve this region and, if anything, cholinergic activation in the hippocampus can itself lead to some PPI disruption (Caine et al, 1991(Caine et al, , 1992Zhang et al, 2000).…”