Delayed neuronal migration of protein kinase Cgamma immunoreactive cells in hippocampal CA1 area after 48 h of moderate hypoxemia in the near term ovine fetus.

The brain is uniquely sensitive to disturbances in energy and oxygen supply, particularly during the early stage of life. Since hypoxemia can indirectly activate the intracellular messenger protein kinase C (PKC), we studied the PKCgamma-immunoreaction in the fetal hippocampal CA1 region of naive (n=4), instrumented control (n=7), and instrumented hypoxemic fetuses (n=14), at a mean gestational age of 127 days. Forty-eight hours of mild to moderate hypoxemia, were followed by a 48-h recovery period. Hypoxemia resulted in an increase in carotid blood flow (137% of control), and a shift towards a higher percentage of high-voltage electrocortical activity. After recovery, the fetal brain was fixated by perfusion of both carotid arteries, sectioned and immunostained for PKCgamma. The distribution of PKCgamma-immunoreactive cells was significantly changed after 48 h of hypoxemia in that the migration of cells (from the ventricular region towards the stratum pyramidale) was delayed (p<0.01) compared to naive and instrumented control animals. In contrast to the distribution, the relative total optical density of PKCgamma-ir cells and fibres in the CA1 hippocampal area was not significant different between the animal groups. We conclude that hypoxemia delayed migration of PKCgamma-ir cells, without neuronal degeneration.