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  • Title: NAD+ attenuates bilirubin-induced augmentation of voltage-gated calcium currents in neurons of the ventral cochlear nucleus.
    Author: Liang M, Liu H, Yin X, Gong L, Jie H, Wang L, Shi H, He J, Chen P, Lu J, Yin S, Yang J.
    Journal: Neurosci Lett; 2022 Jul 27; 784():136747. PubMed ID: 35724761.
    Abstract:
    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.
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