ArticleMolecular brain2017
Ketamine-induced apoptosis in the mouse cerebral cortex follows similar characteristic of physiological apoptosis and can be regulated by neuronal activity.
Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Compensatory attenuation of cortical apoptosis by SK2 downregulation following ketamine anesthesia.Frontiers in pharmacology · 2026Article
- Gastrodin Mitigates Ketamine-Induced Inhibition of F-Actin Remodeling and Cell Migration by Regulating the Rho Signaling Pathway.Biomedicines · 2025Article
- Whole-brain characterization of apoptosis after sevoflurane anesthesia reveals neuronal cell death patterns in the mouse neonatal neocortex.Scientific reports · 2023Article
- Article
- The Association between Hypoxia-Induced Low Activity and Apoptosis Strongly Resembles That between TTX-Induced Silencing and Apoptosis.International journal of molecular sciences · 2022Article
- Sevoflurane-Induced Apoptosis in the Mouse Cerebral Cortex Follows Similar Characteristics of Physiological Apoptosis.Frontiers in molecular neuroscience · 2022Article
- Midazolam Exposure Impedes Oligodendrocyte Development via the Translocator Protein and Impairs Myelination in Larval Zebrafish.Molecular neurobiology · 2022Article
- HDAC6 is critical for ketamine-induced impairment of dendritic and spine growth in GABAergic projection neurons.Acta pharmacologica Sinica · 2021Article
- Ketamine: Neuroprotective or Neurotoxic?Frontiers in neuroscience · 2021Review
- Ketamine and Calcium Signaling-A Crosstalk for Neuronal Physiology and Pathology.International journal of molecular sciences · 2020Review
- The γ-Protocadherins Regulate the Survival of GABAergic Interneurons during Developmental Cell Death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Glutamate controls vessel-associated migration of GABA interneurons from the pial migratory route via NMDA receptors and endothelial protease activation.Cellular and molecular life sciences : CMLS · 2020Article
- Neonatal ketamine exposure-induced hippocampal neuroapoptosis in the developing brain impairs adult spatial learning ability.Neural regeneration research · 2020Article
- Neuronal and peripheral damages induced by synthetic psychoactive substances: an update of recent findings from human and animal studies.Neural regeneration research · 2020Review
- Ketamine Regulates Phosphorylation of CRMP2 To Mediate Dendritic Spine Plasticity.Journal of molecular neuroscience : MN · 2020Article
- LncRNA KCNQ1OT1 Sponges miR-206 to Ameliorate Neural Injury Induced by Anesthesia via Up-Regulating BDNF.Drug design, development and therapy · 2020Article
- Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors.Frontiers in molecular neuroscience · 2018Review
- Chemogenetic Recruitment of Specific Interneurons Suppresses Seizure Activity.Frontiers in cellular neuroscience · 2018Article
- Environmental Enrichment Increases Radiation-induced Apoptosis Not Spontaneous Apoptosis in Mouse Intestinal Crypt Cells.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of general anesthetics on inducing neuronal apoptosis during early brain development are well-documented. However, since physiological apoptosis also occurs during this developmental window, it is important to determine whether anesthesia-induced apoptosis targets the same cell population as physiological apoptosis or different cell types altogether. To provide an adequate plane of surgery, ketamine was co-administered with dexmedetomidine. The apoptotic neurons in the mouse primary somatosensory cortex (S1) were quantitated by immunohistochemistry. To explore the effect of neural activity on ketamine-induced apoptosis, the approaches of Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) and an environmental enrichment (EE) were performed. Ketamine-induced apoptosis in S1 is most prominent at postnatal days 5 and 7 (P5 - P7), and becomes insignificant by P12. Physiological and ketamine-induced apoptosis follow similar developmental patterns, mostly comprised of layer V pyramidal neurons at P5 and shifting to mostly layer II to IV GABAergic neurons by P9. Changes in neuronal activity induced by the DREADD system bidirectionally regulated the pattern of ketamine-induced apoptosis, with reduced activity inducing increased apoptosis and shifting the lamination pattern to a more immature form. Importantly, rearing mice in an EE significantly reduced the magnitude of ketamine-induced apoptosis and shifted its developmental pattern to a more mature form. Together, these results demonstrate that lamination pattern and cell-type dependent vulnerability to ketamine-induced apoptosis follow the physiological apoptosis pattern and are age- and activity-dependent. Naturally elevating neuronal activity is a possible method for reducing the adverse effects of general anesthesia.
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