Temperature control can abolish anesthesia‐induced tau hyperphosphorylation and partly reverse anesthesia‐induced cognitive impairment in old mice

Xiao, Huiling; Run, Xiaoqin; Cao, Xu; Su, Ying; Sun, Zhou; Tian, Cheng; Sun, Shan; Liang, Zhihou

doi:10.1111/pcn.12091

Cited by 17 publications

(13 citation statements)

References 43 publications

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“…Cognitive impairment induced by anesthesia might be the most common type in postoperative cognitive disorder, which was found to influence signal pathways dysfunction, such as activation of GSK‐3β . This research was aimed to reveal the role of GSK‐3β inhibition on cognitive impairment induced by SEV anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

Wang

Zhang

et al. 2020

FEBS Open Bio

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Postoperative cognitive dysfunction is a common complication in elderly patients after surgeries involving anesthesia, but the underlying mechanisms are poorly understood. Lithium is a conventional treatment for bipolar disorder, which exerts a neuroprotective role in various diseases by inhibiting glycogen synthase kinase‐3β (GSK‐3β) in the brain and spinal cord. However, it is not known whether lithium chloride (LiCl) can protect against cognitive dysfunction induced by sevoflurane (SEV) anesthesia. Here, we examined the effects of LiCl on SEV‐induced cognitive dysfunction in rats and on SEV‐induced neuron apoptosis. We report that anesthesia with SEV significantly impaired memory performance, induced oxidative stress and hippocampal neuron apoptosis, and stimulated GSK‐3β activity. Treatment with LiCl ameliorated SEV‐induced cognitive disorder in rats by inhibiting the GSK‐3β/β‐catenin signaling pathway. In addition, LiCl reduced hippocampal neuron apoptosis and oxidative stress induced by SEV anesthesia. These results suggest that LiCl may have potential for development into a therapeutic agent for treatment of SEV anesthesia‐induced cognitive dysfunction.

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Section: Discussionmentioning

confidence: 99%

Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

Wang

Zhang

et al. 2020

FEBS Open Bio

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“…Many rodent studies have demonstrated different experimental outcomes due to differences in body temperature under anesthesia, including studies of the heart, brain, liver, and urogenital system. 16,77,85,95,111,119,137 The technique used to measure body temperature is critical to the interpretation of an experiment, due to the heterogeneity of temperature in different locations of the animal's body, ranging from the temperature of the tail to the animal's true core temperature. The most traditional measurement of the core temperature is the use of direct rectal thermography by either a thermocouple or thermistor.…”

Section: Monitoring Body Temperature and Thermogenic Support Devicesmentioning

confidence: 99%

Effects of Rodent Thermoregulation on Animal Models in the Research Environment

et al. 2018

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The thermal biology of laboratory mice encompasses a robust, dynamic, and multifaceted mixture of behavior and physiology. Physical and physiologic adaptations provide the remarkable capacity for mice to survive in temperatures as low as 4 °C and as high as 43 °C. 54,89 Comprehension of these complex systems necessitates a clear definition and solid understanding of the murine thermoneutral zone (TNZ), which is the range of temperatures across which the resting metabolic rate of heat production is at equilibrium with the animal's evaporative heat loss to the surrounding environment. 14,54 Within the TNZ, animals can maintain stable core body temperatures by responsive behaviors, peripheral vessel diameter, and body postures. 54 The overall mouse TNZ is bound by the lower and upper critical temperature limits, beyond which mice must engage in heating or cooling adjustments, respectively; further definition of these critical temperatures is provided in a glossary of terms for thermal physiology. 22 TNZ is determined by body size and weight, morphology, condition, and resting metabolic rate and is particularly narrow in mice, spanning just 1 to 3 °C, because of a large surface-to-volume ratio and meager body insulation (for example, body hair). 54,74,120 These responses to the ambient environment lead to dramatic increases in metabolic rate and alterations in thermal profiles (Figure 1). 14,54 Long-term (chronic) cold-induced exposures for mice often alter experimental results, described across multiple disciplines. 8,10,27,92,118,129 As a result, the biomedical scientific community has asserted the need to account for and better support the thermal biology of mice, 35,40,65,75,92 although dissenting opinions on this matter have been expressed. 127 Unlike many large endotherms, mice do not have stable core temperatures. Their body temperature oscillates over short bursts of approximately 1 °C even within the TNZ. Mice also show circadian fluctuations in their core temperatures and sleep patterns at standard housing temperatures: mice in barren caging conditions at 23.5 °C maintain a core body temperature of 36.2 °C during the light cycle and 37.5 °C during the dark cycle. 48,72 When provided with deep bedding for nesting, light cycle core temperatures increase to an average 37.2 °C, while the dark cycle temperatures remain at 37.5 °C. 48 The mouse's core temperature and related physiologic state should not be attributed to a static number but instead should be viewed as a dynamic value dependent on environmental context. Over many generations of exposure to particular conditions, mice acclimate through the development of anatomic differences based on their rearing temperatures. Mice raised in colder environments grow significantly shorter tails 55 and ears, 4 have longer fur for increased insulation, 4,60 develop larger livers and kidneys 55 and bones, 3 and have larger deposits of brown adipose tissue (BAT) with increased thermogenic capacity. 63,89 The evolutionary strategy of energy conservation through environme...

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“…administration of insulin or deoxyglucose (Planel et al, 2004). Also, PP-Tau induction was suppressed in mice that were kept euthermic while under general anesthesia (Xiao et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation and Dephosphorylation of Tau Protein During Synthetic Torpor

et al. 2019

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Tau protein is of primary importance for many physiological processes in neurons, where it affects the dynamics of the microtubule system. When hyperphosphorylated (PP-Tau), Tau monomers detach from microtubules and tend to aggregate firstly in oligomers, and then in neurofibrillary tangles, as it occurs in a group of neurodegenerative disorders named thauopathies. A hypothermia-related accumulation of PP-Tau, which is quickly reversed after the return to normothermia, has been shown to occur in the brain of hibernators during torpor. Since, recently, in our lab, a hypothermic torpor-like condition (synthetic torpor, ST) was pharmacologically induced in the rat, a non-hibernator, the aim of the present work was to assess whether ST can lead to a reversible PP-Tau accumulation in the rat brain. PP-Tau was immunohistochemically assessed by staining for AT8 (phosphorylated Tau) and Tau-1 (non-phosphorylated Tau) in 19 brain structures, which were chosen mostly due to their involvement in the regulation of autonomic and cognitive functions in relation to behavioral states. During ST, AT8 staining was strongly expressed throughout the brain, while Tau-1 staining was reduced compared to control conditions. During the following recovery period, AT8 staining progressively reduced close to zero after 6 h from ST. However, Tau-1 staining remained low even after 38 h from ST. Thus, overall, these results show that ST induced an accumulation of PP-Tau that was, apparently, only partially reversed to normal during the recovery period. While the accumulation of PP-Tau may only depend on the physicochemical characteristics of the enzymes regulating Tau phosphorylation, the reverse process of dephosphorylation should be actively regulated, also in non-hibernators. In conclusion, in this work a reversible and widespread PP-Tau accumulation has been induced through a procedure that leads a non-hibernator to a degree of reversible hypothermia, which is comparable to that observed in hibernators. Therefore, the physiological mechanism involved in this process can sustain an adaptive neuronal response to extreme conditions, which may however lead to neurodegeneration when particular intensities and durations are exceeded.

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Temperature control can abolish anesthesia‐induced tau hyperphosphorylation and partly reverse anesthesia‐induced cognitive impairment in old mice

Cited by 17 publications

References 43 publications

Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

Lithium chloride ameliorates cognition dysfunction induced by sevoflurane anesthesia in rats

Effects of Rodent Thermoregulation on Animal Models in the Research Environment

Phosphorylation and Dephosphorylation of Tau Protein During Synthetic Torpor

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