Prenatal hypoxia impairs memory function but does not result in overt structural alterations in the postnatal chick brain

Brain Res Dev Brain Res. 2005 Nov 7;160(1):9-18. doi: 10.1016/j.devbrainres.2005.07.015. Epub 2005 Sep 9.

Abstract

We showed previously that hypoxia in ovo impairs memory consolidation in the chick tested 2 days after hatching. Our present aim was to investigate whether we could detect any morphological effects of the same prenatal hypoxia. Hypoxia was induced by half-wrapping the egg with an impermeable membrane from either days 10-18 (W10-18 chicks) or days 14-18 (W14-18 chicks) of incubation (hatching approximately 21 days). Measurement of blood gases showed that reducing the surface area of the egg for gas exchange resulted in reduced pO2 and increased pCO2 2 days after wrapping. Although this hypoxia was sufficient to impair cognitive processing in the postnatal chick, our data suggest that it did not produce overt structural alterations or changes in the number of neurons, glutamine synthetase-immunoreactive cells or immunoreactivity to synaptophysin in the presynaptic vesicles in the multimodal integration (cortical) area compared to controls. Hence, we found no differences in the astrocyte to neuron ratio, synaptic density and/or vesicle number. Analysis of the ontogeny of astrocytes during the prenatal period of hypoxia showed them to be present at embryonic day 12, but not at the earlier ages examined. Although we found cognitive deficits in chicks from embryos made hypoxic during incubation, our regimen of prenatal hypoxia did not alter any of the parameters measured in the brains. This does not preclude the possibility that changes have occurred at the cellular or molecular levels or in specific neurotransmitter systems.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain Infarction / etiology
  • Brain Infarction / pathology
  • Brain Infarction / physiopathology*
  • Chick Embryo
  • Chickens
  • Disease Models, Animal
  • Fetal Hypoxia / pathology
  • Fetal Hypoxia / physiopathology*
  • Glutamate-Ammonia Ligase / metabolism
  • Glutamic Acid / metabolism
  • Hypoxia, Brain / pathology
  • Hypoxia, Brain / physiopathology*
  • Immunohistochemistry
  • Memory Disorders / etiology
  • Memory Disorders / pathology
  • Memory Disorders / physiopathology*
  • Microscopy, Electron, Transmission
  • Presynaptic Terminals / metabolism
  • Presynaptic Terminals / ultrastructure
  • Synaptic Vesicles / metabolism
  • Synaptic Vesicles / ultrastructure
  • Synaptophysin / metabolism

Substances

  • Synaptophysin
  • Glutamic Acid
  • Glutamate-Ammonia Ligase