Maternal anesthesia and fetal neurodevelopment

Palanisamy, Arvind

doi:10.1016/j.ijoa.2012.01.005

Cited by 89 publications

(78 citation statements)

References 118 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…synaptogenesis, which continues postnatally. 2,3 By birth, most neurons have migrated to their final location in the brain. 2 The formation of the synapses is dependent on electrochemical activity, and involves the activation of calcium channels.…”

Section: Brain Development In the Humanmentioning

confidence: 99%

“…2 The formation of the synapses is dependent on electrochemical activity, and involves the activation of calcium channels. 3 Neurogenesis and synaptogenesis are activity dependent: "Neurons that fire together, wire together". 2 The peak period of myelination occurs during the first two years after birth, during which period the brain structure drastically changes its biochemical composition.…”

Section: Brain Development In the Humanmentioning

confidence: 99%

“…Neurogenesis and neuronal migration accelerate and reach a peak during and after the second trimester of pregnancy. 3 …”

Section: Brain Development In the Humanmentioning

confidence: 99%

“…The lifespan of a rodent is approximately three years, and synaptogenesis occurs mainly after birth. 3 Therefore, the neuron lifespan of a rodent is a maximum of three years, in comparison with the human neuron lifespan, which may be over 100 years. 6 It is important to recognise that the anaesthetic exposure of a rat is equivalent to a much longer exposure in humans.…”

Section: Animal Studiesmentioning

confidence: 99%

“…An anaesthetic exposure of six hours in the pregnant rat, extrapolated to the human, represents over 48 hours of anaesthesia exposure in the pregnant human, and thus may only be relevant in intensive care sedation settings. 3 Evidence in animal models indicates long-term neurodevelopment deficiencies following anaesthesia exposure. Exposure of the infant rat to commonly used anaesthetics (midazolam, N 2 O and isoflurane) in clinically relevant dosages caused widespread apoptotic neurodegeneration in the brain, as well as persistent memory and learning impairment.…”

Section: Animal Studiesmentioning

confidence: 99%

See 4 more Smart Citations

Anaesthesia and the developing brain

Prozesky

2014

Southern African Journal of Anaesthesia and Analgesia

View full text Add to dashboard Cite

Increasing concern about the effect of anaesthesia on the infant and young child is being raised by healthcare practitioners, as well as the public. Immature neurons exposed to anaesthesia may lead to apoptosis and long-term neurobehavioural deficits in animals. The majority of anaesthetic agents work by influencing the gamma-aminobutyric acid or N-methyl-D-aspartate receptors and may induce animal neuroapoptosis. The search for neuroprotective strategies to reverse or counteract the effect of anaesthesia has not been very successful so far. Dexmedetomidine is an α 2 -adrenergic receptor and may have neuroprotective effects. Available human studies have failed to prove any long-term neurobehavioural deficiencies caused by anaesthetic exposure. Large international prospective studies are currently underway that may change the practice of paediatric and obstetric anaesthesiologists in the future.

show abstract

Section: Brain Development In the Humanmentioning

confidence: 99%

Section: Brain Development In the Humanmentioning

confidence: 99%

“…Neurogenesis and neuronal migration accelerate and reach a peak during and after the second trimester of pregnancy. 3 …”

Section: Brain Development In the Humanmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

See 3 more Smart Citations

Anaesthesia and the developing brain

Prozesky

2014

Southern African Journal of Anaesthesia and Analgesia

View full text Add to dashboard Cite

show abstract

Sevoflurane anesthesia represses neurogenesis of hippocampus neural stem cells via regulating microRNA‐183‐mediated NR4A2 in newborn rats

Shao

Xia

2018

Journal Cellular Physiology

View full text Add to dashboard Cite

Sevoflurane has been commonly utilized in nonobstetric surgeries in pregnant women, and its impacts on fetal brain are still not completely known. Ectopic NR4A2 expression has been reported to be related with familial Parkinson disease, and through dual luciferase we found that NR4A2 is a target gene of microRNA-183 (miR-183). We proposed a hypothesis that miR-183 may participate in the process by targeting NR4A2 in neurons after sevoflurane anesthesia. To verify the effect of sevoflurane on hippocampal neural stem cells (NSCs) proliferation and differentiation, we conducted EdU assay and immunofluorescence staining. Next, for better understanding of the impact of miR-183, we altered the miR-183 expression using mimic and inhibitor. Meanwhile, the targeting relationship between miR-183 and NR4A2 was validated by a bioinformatics website and dual-luciferase reporter gene assay. Finally, expressions of miR-184, NR4A2, SRY (sex-determining region Y)-box 2 (Sox2), and brain-derived neurotrophic factor (BDNF) were determined and evaluated by reverse transcription quantitative polymerase chain reaction and western blot analysis. First, sevoflurane was determined a crucial factor in biological behaviors of hippocampal NSCs. Moreover, upregulated miR-183 expression by mimic inhibited the proliferation and differentiation of NSCs. Sevoflurane negatively regulated NR4A2 and Sox2 expressions but positively regulated miR-183 and BDNF expressions. Our findings revealed the underlying novel mechanism by which sevoflurane inhibits hippocampal NSC proliferation and differentiation through interaction with miR-183 and NR4A2. The study provides reliable reference for safe application of sevoflurane anesthesia in neonates.

show abstract

Fetally‐injected drugs for immobilization and analgesia do not modify fetal brain development in a rabbit model

et al. 2021

View full text Add to dashboard Cite

Objective During fetal surgery, fetuses receive medication (atropine‐fentanyl‐curare) to prevent fetal pain, movement and bradycardia. Although essential there has been no detailed review of potential side effects. Herein we aimed to assess the effects of this medication cocktail on fetal brain development in a rabbit model. Methods Pregnant does underwent laparotomy at 28 days of gestation. Two pups of each horn were randomized to an ultrasound guided injection with medication (atropine‐cisatracurium‐fentanyl, as clinically used) or saline (sham). The third pup was used as control. At term, does were delivered by cesarean. Outcome measures were neonatal biometry, neuromotoric functioning and neuro‐histology (neuron density, synaptic density and proliferation). Results Maternal vital parameters remained stable during surgery. Fetal heart rates did not differ before and after injection, and were comparable for the three groups. At birth, neonatal body weights and brain‐to‐body weight ratios were also comparable. Both motor and sensory neurobehavioral scores were comparable. There were no differences in neuron density or proliferation. Sham pups, had a lower synaptic density in the hippocampus as compared to the medication group, however there was no difference in the other brain areas. Conclusion In the rabbit model, fetal medication does not appear to lead to short‐term neurocognitive effects.

show abstract

Maternal anesthesia and fetal neurodevelopment

Cited by 89 publications

References 118 publications

Anaesthesia and the developing brain

Anaesthesia and the developing brain

Sevoflurane anesthesia represses neurogenesis of hippocampus neural stem cells via regulating microRNA‐183‐mediated NR4A2 in newborn rats

Fetally‐injected drugs for immobilization and analgesia do not modify fetal brain development in a rabbit model

Contact Info

Product

Resources

About