Object memory in young and aged mice after sevoflurane anaesthesia

Wiklund, Andreas; Granon, Sylvie; Fauré, Philippe; Sundman, Eva; Changeux, Jean‐Pierre; Eriksson, Lars

doi:10.1097/wnr.0b013e328330cd2b

Cited by 32 publications

(21 citation statements)

References 108 publications

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“…In addition, β2 KO showed increased neurodegeneration during aging (Picciotto et al, 2000;Zoli et al, 1999). Contradictory results exist about memory impairment in β2 KO mice, Wiklund et al (2009) did not identify any impairment. On the other hand some authors found spatial learning deficits (Levin et al, 2009).…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 66%

A role for β2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus

Lombardo

Catteau

Besson

et al. 2016

Neurobiology of Aging

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Alzheimer's disease (AD) is characterized by the presence of plaques and tangles. Only certain brain regions are vulnerable to progressive neurodegeneration. It is therefore important to study the contribution of key brain structures to AD pathology. Here, we investigated the consequences of amyloid accumulation specifically in dentate gyrus (DG). This was obtained with viral transduction of human amyloid precursor protein harboring 3 pathogenic mutations (hAPP-SLA, Swedish, London, and Austrian) in DG. Adult wild-type C57Bl/6J mice exhibited long-term expression of hAPP-SLA, synthesis and deposition of oligomeric amyloid beta (Aβ), and associated memory impairment. We then investigated the role of α7 or β2 subunits of the nicotinic acetylcholine receptor by transducing hAPP-SLA into C57Bl/6J mice knock-out (KO) for α7 or β2 subunits. β2 KO mice did not exhibit memory loss induced by hAPP-SLA expression, whereas aged mice lacking the α7 subunit displayed a hAPP-SLA independent cognitive deficit. The present data reveal a role for β2 containing nicotinic acetylcholine receptors in the memory deficits associated with DG specific amyloid beta expression.

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 66%

A role for β2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus

Lombardo

Catteau

Besson

et al. 2016

Neurobiology of Aging

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“…Evidences from animal models suggested volatile anesthetics interaction with neurodegenerative mechanisms, such as the onset and progression of Alzheimer’s disease [5], [16], [17]. Sevoflurane is one of the most commonly used volatile anesthetics and it had been shown to impair long-term emotional memory consolidation in human research [18], and especially in old mice [19]. But the underlying molecular mechanisms are still unknown.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane Induces Endoplasmic Reticulum Stress Mediated Apoptosis in Hippocampal Neurons of Aging Rats

et al. 2013

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Elderly patients are more likely to suffer from postoperative memory impairment for volatile anesthetics could induce aging neurons degeneration and apoptosis while the mechanism was still elusive. Therefore we hypothesized that ER stress mediated hippocampal neurons apoptosis might play an important role in the mechanism of sevoflurane-induced cognitive impairment in aged rats. Thirty 18-month-old male Sprague-Dawley rats were divided into two groups: the sham anesthesia group (exposure to simply humidified 30–50% O2 balanced by N2 in an acrylic anesthetizing chamber for 5 hours) and the sevoflurane anesthesia group (received 2% sevoflurane in the same humidified mixed air in an identical chamber for the same time). Spatial memory of rats was assayed by the Morris water maze test. The ultrastructure of the hippocampus was observed by transmission electron microscopy (TEM). The expressions of C/EBP homologous protein (CHOP) and caspase-12 in the hippocampus were observed by immunohistochemistry and real-time PCR analysis. The apoptosis neurons were also assessed by TUNEL assay. The Morris water maze test showed that sevoflurane anesthesia induced spatial memory impairment in aging rats (P<0.05). The apoptotic neurons were condensed and had clumped chromatin with fragmentation of the nuclear membrane, verifying apoptotic degeneration in the sevoflurane group rats by TEM observation. The expressions of CHOP and caspase-12 increased, and the number of TUNEL positive cells of the hippocampus also increased in the sevoflurane group rats (P<0.05). The present results suggested that the long time exposure of sevoflurane could induce neuronal degeneration and cognitive impairment in aging rats. The ER stress mediated neurons apoptosis may play a role in the sevoflurane-induced memory impairment in aging rats.

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“…There is no standard time span to assess the short‐term learning and memory after anesthesia. Previous studies reported that the tests are initiated 24 h , 48 h or 1 week after anesthesia. Sevoflurane and desflurane are cleared from the brain within minutes after the discontinuation of inhalation .…”

Section: Discussionmentioning

confidence: 99%

“…There are no clinically relevant standard neuropsychological tests to determine the incidence of POCD. Furthermore, the use of very different test methods in animal studies led to the emergence of inconsistent results .…”

Section: Introductionmentioning

confidence: 99%

Single and repeated sevoflurane or desflurane exposure does not impair spatial memory performance of young adult mice

Kılıçaslan

Belviranlı

Okudan

et al. 2013

Fundamemntal Clinical Pharma

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Volatile anesthetics are known to disturb the spatial memory in aged rodents, but there is insufficient information on their effects on young adult rodents. The aim of this study was to compare the effects of single and repeated exposure to desflurane and sevoflurane on spatial learning and memory functions in young adult mice. Balb/c mice (2 months old) were randomly divided into six equal groups (n = 8). The groups with single inhalation were exposed to 3.3% sevoflurane or 7.8% desflurane or vehicle gas for 4 h, respectively. The groups with repeated inhalation were exposed to 3.3% sevoflurane or 7.8% desflurane or vehicle gas for 2 h a day during 5 consecutive days. Spatial learning and memory were tested in the Morris water maze 24 h after exposure. In the learning phase, the parameters associated with finding the hidden platform and swimming speed, and in the memory phase, time spent in the target quadrant and the adjacent quadrants, were assessed and compared between the groups. In the 4-day learning process, there was no significant difference between the groups in terms of mean latency to platform, mean distance traveled and average speed (P > 0.05). During the memory-test phase, all mice exhibited spatial memory, but there was no significant difference between the groups in terms of time spent in the target quadrant (P > 0.05). Sevoflurane and desflurane anesthesia did not impair acquisition learning and retention memory in young adult mice.

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Object memory in young and aged mice after sevoflurane anaesthesia

Cited by 32 publications

References 108 publications

A role for β2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus

A role for β2* nicotinic receptors in a model of local amyloid pathology induced in dentate gyrus

Sevoflurane Induces Endoplasmic Reticulum Stress Mediated Apoptosis in Hippocampal Neurons of Aging Rats

Single and repeated sevoflurane or desflurane exposure does not impair spatial memory performance of young adult mice

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