ArticleFrontiers in pharmacology2026
Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: A single exposure to general anesthetic can induce acute increase in neuronal apoptosis of the neonatal brain; however, how the brain counteracts the anesthetic-induced neurotoxicity remains unknown. The aim of this study is to explore how the neonatal cerebral cortex responds to anesthetic-induced neuronal apoptosis and the underlying mechanisms involved. Materials and Methods: Postnatal day 7 rats received intraperitoneal ketamine injections. Apoptotic neurons in the primary somatosensory cortex (S1) were quantified via immunohistochemistry. Whole-cell patch-clamp recordings were performed to assess neuronal activity of pyramidal neurons, including small conductance Ca Results: Ketamine induced an acute surge in S1 neuronal apoptosis (mean ± SEM, control vs. ketamine, 1386.11 ± 253.63/mm Conclusion: The developing cortex compensates for ketamine-induced neuronal apoptosis by suppressing subsequent physiological apoptosis. This anti-apoptotic response is critically mediated by increased neuronal activity, driven by UPS-dependent SK2 downregulation.
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