Brainstem monoamine pathology of neonatal hypoxic–ischemic brain damage: A model of acute stage of neonatal asphyxia

Abstract Neonatal hypoxic–ischemic encephalopathy (HIE) is one of the most severe perinatal diseases and leads to high mortality and sometimes severe neurological sequelae. At the acute stage of HIE, it is thought to be the damage of catecholaminergic system in the brainstem. And then, HIE reflects mental development throughout the norepinephrine and serotonin systems, which mainly originates in the brainstem. Therefore, we studied both systems in the brainstem of neonatal HIE model rats with tyrosine hydroxylase (TH) and tryptophan hydroxylase (TpH) immunohistochemistry and a high-performance liquid column (HPLC) to measure norepinephrine and serotonin and their metabolism. As a result, the TH-positive and TpH-positive cell numbers significantly decreased 2 days after hypoxic–ischemic (HI) insult ( n = 10). However, 7 days after insult ( n = 10), the TH-positive and TpH-positive cell numbers had recovered in most regions. HPLC demonstrated a significant difference in the norepinephrine concentration 2 days after HI insult, but not in the other monoamines.