ArticleActa pharmacologica Sinica2021
HDAC6 is critical for ketamine-induced impairment of dendritic and spine growth in GABAergic projection neurons.
Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- Epigenetic mechanisms of rapid-acting antidepressants.Translational psychiatry · 2024Review
- Ketamine impairs growth cone and synaptogenesis in human GABAergic projection neurons via GSK-3β and HDAC6 signaling.Molecular psychiatry · 2024Article
- Changes in synaptic markers after administration of ketamine or psychedelics: a systematic scoping review.Frontiers in psychiatry · 2023Article
- Epigenetic Mechanisms of Postoperative Cognitive Impairment Induced by Anesthesia and Neuroinflammation.Cells · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Ketamine is widely used in infants and children for anesthesia; both anesthetic and sub-anesthetic doses of ketamine have been reported to preferentially inhibit the GABAergic neurons. Medium spiny neurons (MSNs), the GABAergic projection neurons in the striatum, are vulnerable to anesthetic exposure in the newborn brain. Growth of dendrites requires a deacetylase to remove acetyl from tubulin in the growth cone to destabilize the tubulin. Histone deacetylase 6 (HDAC6) affects microtubule dynamics, which are involved in neurite elongation. In this study we used a human induced pluripotent stem cells (iPSCs)-derived striatal GABA neuron system to investigate the effects of ketamine on HDAC6 and the morphological development of MSNs. We showed that exposure to ketamine (1-500 μM) decreased dendritic growth, dendrite branches, and dendritic spine density in MSNs in a time- and concentration-dependent manner. We revealed that ketamine treatment concentration-dependently inhibited the expression of HDAC6 or aberrantly translocated HDAC6 into the nucleus. Ketamine inhibition on HDAC6 resulted in α-tubulin hyperacetylation, consequently increasing the stability of microtubules and delaying the dendritic growth of MSNs. Finally, we showed that the effects of a single-dose exposure on MSNs were reversible and lasted for at least 10 days. This study reveals a novel role of HDAC6 as a regulator for ketamine-induced deficits in the morphological development of MSNs and provides an innovative method for prevention and treatment with respect to ketamine clinical applications.
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