Effects of ketamine on voltage-gated sodium channels in the barrel cortex and the ventral posteromedial nucleus slices of rats. Issue 17 (10th December 2019)

• Record Type: Journal Article
• Authors: Yin, Jianyin; Fu, Bao; Wang, Yuan; Yu, Tian
• Is Part Of: NeuroReport. Volume 30:Issue 17(2019)
• Publication Date: 2019-12-10
• Subjects: general anesthesia -- inactivation -- ketamine -- sodium channel -- thalamocortical; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000001344
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : Ketamine is commonly used as a dissociative anesthetic with unique actions in the central nervous system. Previous studies have found that the thalamocortical systems play an important role in general anesthetics induced unconsciousness. Whether the voltage-gated sodium channels in the thalamocortical systems are the target of ketamine remain unclear. The present study used a whole-cell patch-clamp technique to observe the effects of ketamine on voltage-gated Na + channels in thalamocortical pyramidal neurons. We found that IC50 of ketamine on Na + currents in the primary somatosensory barrel cortex pyramidal neurons and the thalamus ventral posteromedial nucleus pyramidal neurons was 686.72 ± 39.92 and 842.65 ± 87.28 μM, respectively. Ketamine accelerated the Na + channels inactivation and slowed inactivation of Na + channels after recovery but did not affect the activation. We demonstrated the detailed suppression process of neural voltage-gated Na + channels by ketamine on thalamocortical slice. This may provide a new insight into the mechanical explanation for the ketamine anesthesia. Abstract : Supplemental Digital Content is available in the text.