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Abstract Neonatal hyperbilirubinemia in newborn infants results from a predisposition of the production of bilirubin and their limited ability to excrete it. Deposition of bilirubin in the neuron membrane causes permanent neuronal injury. Considering the affinity of bilirubin molecule to phospholipids of the plasma membrane, the sequence of membrane events initiated by bilirubin molecules damages all adjacent membrane-bound enzymes and receptors.The results are accentuation of bilirubin uptake and disturbance of certain plasma membrane functions (e.g., glutamate transport). Impairment of glutamate transport in neurons causes an increase in the extracellular glutamate.Glutamate is a principal excitatory neurotransmitter present at synaptic junctions and is essential in cognitive functioning. However, excess glutamate can lead to neuronal damage and cell death via increased intracellular calcium concentrations. |