Asphyxia induced by umbilical cord occlusion alters glutamatergic and GABAergic synaptic transmission in neurons of the superior colliculus in fetal rats

• Fetal brain asphyxia in rats was induced by umbilical cord occlusion.
• Asphyxia increased [Cl−]i and [Ca2+]i in fetal superior colliculus.
• Asphyxia induced a shift in GABA action from Cl− influx to efflux.
• The [Ca2+]i rise was mediated by both NMDA and non-NMDA receptors.
• Synaptically induced increase in [Ca2+]i was attenuated after acute asphyxia.

Using optical recordings, we studied the effects of asphyxia on intracellular Cl− and Ca2+ concentrations ([Cl−]i; [Ca2+]i) in the superior colliculus of fetal rats, which were connected via the umbilical cord to the dam. Acute asphyxia was induced by umbilical cord occlusion. The number of fetal superior colliculus neurons showing GABA-mediated increases in [Cl−]i (leading to hyperpolarization) following local synaptic electrical stimulation had decreased by 3 h post-asphyxiation, while the number showing GABA-mediated decreases in [Cl−]i (leading to depolarization) increased. [Ca2+]i rise, which occurred after acute asphyxiation, was antagonized by both non-NMDA and NMDA receptor antagonists. The increase in [Ca2+]i following focal superior colliculus stimulation was markedly attenuated at 3 h post-asphyxiation.These findings suggest that asphyxia induced by umbilical occlusion induces changes in glutamatergic and GABAergic synaptic transmission in the fetal brain.