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Updated: Jun 13, 2026

Adaptation of Microelectrode Array Technology for the Study of Anesthesia-induced Neurotoxicity in the Intact Piglet Brain
Published on: May 12, 2018
AMPK attenuates bupivacaine-induced neurotoxicity
1Department of Dental Anesthesiology and Dental Research Institute, School of Dentistry, Seoul National University, 28 Yeongeon-dong Jongno-gu, Seoul 110-768, Republic of Korea.
Abstract:
Bupivacaine has been widely used as a long-acting local anesthetic. However, evidence strongly suggests that bupivacaine causes apoptosis. AMP-activated protein kinase (AMPK) regulates metabolic homeostasis and mediates cellular protection from stress. We hypothesized that AMPK may be cytoprotective in bupivacaine-treated Schwann cells. To explore this, we applied bupivacaine to the RT4-D6P2T Schwann cell line. The expression of phosphorylated AMPK was compared after bupivacaine treatment. Bupivacaine induced cell death in a time- and dose- [50% lethal dose (LD(50)) = 316 microM] dependent manner, and increased expression of phosphorylated AMPK after bupivacaine treatment. Bupivacaine-induced cytotoxicity was attenuated by AICAR (an AMPK activator), whereas compound C (an AMPK inhibitor) enhanced it. The cytoprotective effect of AICAR was reversed in the presence of iodotubercidin, an AICAR inhibitor. Our results suggest that the AMPK pathway may protect Schwann cells from bupivacaine-induced cytotoxicity.
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