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Published on: May 12, 2018
Heightened stress response and cognitive impairment after repeated neonatal sevoflurane exposures might be linked to
Guanghai Liu1, Tiangui Zhu1, Aihua Zhang1
1Department of Anesthesiology, The First People's Hospital of Yancheng, Yancheng, 224005, Jiangsu, People's Republic of China.
Insights
Repeated sevoflurane anesthesia in young rats impairs learning and memory. Bumetanide treatment protected against these effects by reducing stress responses linked to GABAergic signaling.
Area of Science:
- Neuroscience
- Anesthesiology
- Developmental Biology
Background:
- Early-life exposure to anesthesia is linked to cognitive deficits.
- Developmental changes in GABA type A receptors (GABAARs) are implicated in neurodevelopmental disorders.
Purpose of the Study:
- To investigate the role of GABAergic signaling in mediating adverse effects of repeated sevoflurane exposure in developing rats.
- To assess the impact of sevoflurane on learning, memory, and stress response.
Main Methods:
- Neonatal Sprague-Dawley male rats received daily sevoflurane exposure.
- A subset of rats were pretreated with bumetanide, a GABAAR inhibitor.
- Cognitive function was assessed using the Morris water maze (MWM).
- Corticosterone levels were measured to evaluate stress response.
Main Results:
- Repeated sevoflurane exposure caused learning and memory impairment in the MWM.
- Sevoflurane increased corticosterone levels and heightened stress response in rats.
- Bumetanide pretreatment attenuated corticosterone levels, normalized stress response, and prevented cognitive deficits.
Conclusions:
- Heightened stress response and cognitive impairment following early-life sevoflurane exposure may be associated with excessive GABAAR-mediated depolarization.
- Targeting GABAergic signaling with bumetanide offers a potential protective strategy against sevoflurane-induced neurodevelopmental toxicity.
Objective:
Children with repeated exposures to anesthesia at an early age are at an increased risk of cognitive impairment. Data in the literature link increased developmental depolarizing γ-aminobutyric acid (GABA) type A receptor (GABAAR) at younger age to neurodevelopmental disorders. Here we investigated the involvement of GABAergic signaling during development in mediating the adverse effects of repeated sevoflurane exposures.
Methods:
Sprague-Dawley male rats received repeated exposures to 3 % sevoflurane for 2 h daily for 3 consecutive days on postnatal days (P) 4, 5, and 6; maternally separated and unseparated rats served as controls. A subgroup of rats received three injections of the Na(+)-K(+)-2Cl(-) cotransporter inhibitor, bumetanide (1.82 mg/kg, intraperitoneally) 15 min prior to initiation of each sevoflurane exposure.
Results:
The results showed that repeated neonatal sevoflurane exposures contribute to learning and memory impairment in the Morris water maze (MWM) at P60. The corticosterone level was significantly increased immediately after repeated neonatal sevoflurane exposures. Repeated neonatal sevoflurane exposures heightened the secretion of corticosterone in response to stress in P7 and P60 rats. Pretreatment of male rats prior to each sevoflurane exposure with bumetanide attenuated the corticosterone level immediately after repeated neonatal sevoflurane exposures, normalized endocrine response to stress at P7 and P60, and attenuated the sevoflurane-induced learning and memory impairment in the MWM.
Conclusion:
These data suggested that the heightened stress response and cognitive impairment after repeated neonatal sevoflurane exposures might be linked to excessive GABAAR-mediated depolarization.
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