Multiple exposures to sevoflurane across postnatal development may cause cognitive deficits in older age
Yuanping Zhong1, Chao Zhang2, Yi Wang1
1Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, PR China.
Insights
Repeated sevoflurane anesthesia in early life may impair cognitive function in old age. This study found sevoflurane exposure did not affect learning and memory in juvenile or adult rats, but worsened it in aged rats.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- Anesthesia exposure during critical developmental periods raises concerns about long-term neurological effects.
- Understanding the impact of repeated anesthesia on cognitive function across the lifespan is crucial for patient safety.
Purpose of the Study:
- To investigate the long-term effects of repeated sevoflurane anesthesia exposure during postnatal development on cognitive function and related molecular markers.
- To determine if early-life anesthesia exposure influences cognitive performance and neuropathology in juvenile, adult, and aged Sprague-Dawley rats.
Main Methods:
- Newborn Sprague-Dawley rats were exposed to sevoflurane or carrier gas on postnatal days 7, 14, and 21.
- Cognitive function was assessed using the Morris Water Maze (MWM) test at juvenile, adult, and aged stages.
- Hippocampal expression of amyloid precursor protein (APP), microtubule-associated protein tau (Mapt) mRNA, amyloid-beta (Aβ), tau, and phosphorylated tau (P-tau) proteins was analyzed.
Main Results:
- Repeated sevoflurane exposure led to significantly decreased MWM performance in aged rats.
- While APP and Mapt mRNA levels remained unchanged, tau expression increased in the juvenile hippocampus, and P-tau increased in the adult hippocampus.
- Aβ, tau, and P-tau protein levels were upregulated in the hippocampus of aged rats exposed to sevoflurane.
Conclusions:
- Multiple sevoflurane exposures during postnatal development do not impair cognitive function in childhood or adulthood.
- However, repeated sevoflurane exposure can induce or aggravate cognitive impairment in old age.
- The observed cognitive deficits in aged rats may be linked to the overexpression of tau, P-tau, and Aβ proteins in the hippocampus.
Background:
The aim of the study was to determine the effects of repeated anesthesia exposure across postnatal development.
Methods:
Seventy-two newborn Sprague-Dawley rats were randomly divided into Sev group and Con-aged group. Sev groups were exposed to 2.6% sevoflurane for 2 h on postnatal day (P) 7, P14, and P21; the Con groups only received carrier gas for 2 h. Learning and memory were evaluated using the MWM test at P31 (juvenile), P91 (adult), and 18 months postnatally (aged). The relative expression of APP and Mapt mRNA was detected by RT-PCR, while Aβ, tau, and P-tau protein levels were analyzed by immunohistochemistry.
Results:
After repeated inhalation of sevoflurane, MWM test performance was significantly decreased in the Sev-aged group compared to the Con-aged group (P > 0.05). The relative expression of APP and Mapt mRNA was not significantly different between groups in each growth period (P > 0.05). The tau expression in the juvenile hippocampal CA1, CA3, and dentate gyrus regions increased markedly in the Sev group, while P-tau only increased in the hippocampal CA3 region in the Sev-adult group. The expression of tau, P-tau, and Aβ in the hippocampal regions was upregulated in the Sev-aged group.
Conclusions:
Multiple exposures to sevoflurane across postnatal development can induce or aggravate cognitive impairment in old age.
Impact:
Whether multiple sevoflurane exposures across postnatal development cause cognitive impairment in childhood, adulthood, or old age, as well as the relationship between sevoflurane and the hippocampal Aβ, tau, and P-tau proteins, remains unknown. This study's results demonstrate that multiple exposures to sevoflurane across postnatal development do not appear to affect cognitive function in childhood and adulthood; however, multiple exposures may lead to a cognitive function deficit in old age. The underlying mechanism may involve overexpression of the tau, P-tau, and Aβ proteins in the hippocampus.
More Related Videos
09:36Halogenated Agent Delivery in Porcine Model of Acute Respiratory Distress Syndrome via an Intensive Care Unit Type Device
Published on: September 24, 2020
19:57The Use of Trace Eyeblink Classical Conditioning to Assess Hippocampal Dysfunction in a Rat Model of Fetal Alcohol Spectrum Disorders
Published on: August 5, 2017