NAD+ attenuates bilirubin-induced augmentation of voltage-gated calcium currents in neurons of the ventral cochlear nucleus.

Min Liang, Hanwei Liu, Xinlu Yin, Lina Gong, Huiqun Jie, Luyang Wang, Haibo Shi, Jingchun He, Penghui Chen, Jingrong Lu, Shankai Yin, Jun Yang

Neuroscience letters 2022 Jul 27

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Nicotinamide adenine dinucleotide (NAD+) is a ubiquitous molecule with wide-ranging roles in several cell processes, such as regulation of calcium homeostasis and protection against cell injuries. However, the roles of NAD+ in neuroprotection is poorly understood. The main neurons in ventral cochlear nucleus (VCN) are highly susceptible to bilirubin-associated excitotoxicity. We investigated the effects of NAD+ on VCN neurons by whole cell patch-clamp recordings. We found that NAD+ effectively reverses and inhibits bilirubin-mediated enhancement of voltage-gated calcium (VGCC) currents in VCN neurons. Moreover, NAD+ itself did not affect VGCC currents. These results collectively suggest that NAD+ may be neuroprotective by attenuating Ca2+ influx to suppress bilirubin-induced intracellular Ca2+ overloads. Our research provides a basis for evaluation of NAD+ as a promising therapeutic target for bilirubin encephalopathy and excitotoxicity associated with other neurological disorders. Copyright © 2022 Elsevier B.V. All rights reserved.

Citation

Min Liang, Hanwei Liu, Xinlu Yin, Lina Gong, Huiqun Jie, Luyang Wang, Haibo Shi, Jingchun He, Penghui Chen, Jingrong Lu, Shankai Yin, Jun Yang. NAD+ attenuates bilirubin-induced augmentation of voltage-gated calcium currents in neurons of the ventral cochlear nucleus. Neuroscience letters. 2022 Jul 27;784:136747