Article Text

  1. M Itoh1,
  2. M Shiraishi1,
  3. Y Takizawa1
  1. 1Department of Mental Retardation and Birth Defect Research, National Center of Neurology and Psychiatry, Kodaira, Japan


Objective 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 related 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. In the present study, we investigated acute damage of brainstem monoamine system after HI insult.

Methods We made neonatal HIE model rats according to Rice’s method. Animals were kept in a room for 2 days (post-HI day 2) and 7 days (post-HI day 7) after the treatment. We divided four groups, post-HI day 2, post-HI day 7, control day 2 and control day 7. And then, we performed histological examination with tyrosine hydroxylase (TH) and tryptophan hydroxylase (TpH) immunohistochemistry. All experimental protocols were approved by the animal ethical committee of our institute.

Results The TH-positive and TpH-positive cell numbers significantly decreased 2 days after HI insult (N = 10). However, 7 days after insult (N = 10), the TH-positive and TpH-positive cell numbers had recovered in most regions.

Conclusion Neonatal asphyxia may lead to norepinephrinergic autonomic dysfunction of brainstem at the acute stage.

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