Abstract
Recent studies have pointed out that exposure of neonates to anesthetic agents causes acute widespread neurodegeneration and long-lasting neurocognitive dysfunction in rodents. Although acute toxic effects of sevoflurane on cellular viability in the hippocampus have been reported in some studies, little is known about the effects of neonatal anesthesia on long-term hippocampal synaptic plasticity, which has been implicated in the processes of neurocognitive function. We examine the long-term influences of neonatal exposure of pentobarbital, propofol, and sevoflurane on hippocampal synaptic plasticity in rats by using electrophysiological methods. Our data revealed that these agents cause suppression of long-term potentiation (LTP) induction in hippocampal CA1 region lasting into the post-growth period. This persistent change in synaptic plasticity after neonatal anesthesia may be one of the mechanisms underlying anesthetics-induced neurocognitive dysfunctions.
