Maternal hypoxia during pregnancy induces fetal neurodevelopmental brain damage: Partial protection by magnesium sulfate

Hava Golan, I. Kashtuzki, M. Hallak, Y. Sorokin, M. Huleihel

Research output: Contribution to journalArticlepeer-review

47 Scopus citations


Fetal low brain oxygenation may be an outcome of maternal complications during pregnancy and is associated with increased risk of cerebral palsy and periventricular leukomalacia in newborns. One treatment used for prevention of fetal brain damage is maternal treatment with MgSO4. Although this treatment is indicated to reduce the risk of cerebral palsy in newborns, its use remains controversial. We have shown previously that pretreatment with MgSO4 in a mouse model of maternal hypoxia prevented a delay in the development of motor reflexes induced by hypoxia. We demonstrate here that pretreatment with MgSO4 reduces hypoxia-induced motor disabilities in adult offspring. This effect is associated with histologic protection of the Purkinje cells in the cerebellum and stabilization of brain-derived neurotrophic factor (BDNF) levels in the cerebellum. MgSO4 did not prevent the reduction in cerebral cortex cell density and cell size induced by maternal hypoxia, however, nor did it interfere with the modulation of BDNF and nerve growth factor (NGF) expression in the cerebral cortex. MgSO4 pretreatment also prevented the impairment of short-term memory (30 min, P < 0.05) but not long-term memory (7 days). Nevertheless, maternal pretreatment with MgSO4 reduced CA1 cell layer width and induced alterations in both NGF and BDNF in the hippocampus. These results support the prophylactic effect of MgSO4 against motor disabilities; however, they may also indicate possible harmful effects on the cerebral cortex and hippocampus.

Original languageEnglish
Pages (from-to)430-441
Number of pages12
JournalJournal of Neuroscience Research
Issue number3
StatePublished - 1 Nov 2004


  • Hypoxia
  • Magnesium sulfate
  • Neurogenesis
  • Neurotrophic factors

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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