Ketamine, a phencyclidine derivative and -methyl-D-aspartate (NMDA) receptor antagonist, is widely used as an anesthetic, analgesic, and sedative agent in daily pediatric practice. Experimental studies have suggested that early prenatal or postnatal exposure to ketamine can induce neuroapoptosis, and establish neurobehavioral deficits that are evident in adulthood. However, most of the currently available clinical evidence is derived from retrospective and observational clinical studies. We, herein, attempt a brief review of the cellular and molecular mechanisms suggested to mediate ketamine-induced developmental neurotoxicity, utilizing a selected number of recent experimental evidence.
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| http://dx.doi.org/10.4103/joacp.JOACP_415_19 | DOI Listing |
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Increasing evidence suggests that anesthesia may induce developmental neurotoxicity, yet the influence of genetic predispositions associated with congenital anomalies on this toxicity remains largely unknown. Children with congenital heart disease often exhibit mutations in cilia-related genes and ciliary dysfunction, requiring sedation for their catheter or surgical interventions during the neonatal period. Here we demonstrate that briefly exposing ciliopathic neonatal mice to ketamine causes motor skill impairments, which are associated with a baseline deficit in neocortical layer V neuron apical spine density and their altered dynamics during motor learning.
View Article and Find Full Text PDFThe impact of dexmedetomidine on ketamine-induced neurotoxicity and cognitive impairment in young mice.
Int J Dev Neurosci
November 2024
Department of Anesthesiology and Critical Care Medicine, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Article Synopsis
- The study investigates whether dexmedetomidine can protect neurons from damage caused by ketamine, focusing on neurotoxicity and cell death.
- In experiments, dexmedetomidine showed effectiveness in reducing neuron apoptosis but did not improve issues related to neuronal development after ketamine exposure.
- Although dexmedetomidine helps with some neural damage, it doesn't significantly enhance motor coordination or cognitive functions in the tested subjects.
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The mechanism of ketamine-induced neurotoxicity development remains elusive. Mitochondrial fusion/fission dynamics play a critical role in regulating neurogenesis. Therefore, this study was aimed to evaluate whether mitochondrial dynamics were involved in ketamine-induced impairment of neurogenesis in neonatal rats and long-term synaptic plasticity dysfunction.
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J Biochem Mol Toxicol
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College of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
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