Bilirubin enhances the activity of ASIC channels to exacerbate neurotoxicity in neonatal hyperbilirubinemia in mice
Ke Lai, Xing-Lei Song, Haosong Shi, Xin Qi, Chunyan Li, Jia Fang, Fan Wang, Oleksandr Maximyuk, Oleg Krishtal, Tian‐Le Xu, Xiaoyan Li, Kun Ni, Wanpeng Li, Hai-Bo Shi, Lu‐Yang Wang, Shankai Yin
Abstract
concentration, spike firings, and cell death. Furthermore, neonatal conditioning with concurrent hyperbilirubinemia and hypoxia-induced acidosis promoted long-term impairments in learning and memory and complex sensorimotor functions in vivo, which are largely attenuated in ASIC1a null mice. These findings suggest that targeting acidosis and ASICs may attenuate neonatal hyperbilirubinemia complications.
Topics & Concepts
NeurotoxicityPharmacologyBilirubinMedicineNeuroscienceChemistryInternal medicineBiologyToxicityNeonatal Health and BiochemistryMetabolism and Genetic DisordersHeme Oxygenase-1 and Carbon Monoxide