The neuronal toxicity of general anesthetics on the developing rat brain

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It was recently shown that exposure of commonly used general anesthetics to the developing rat brain during the peak of synaptogenesis can trigger widespread apoptotic neurodegeneration in the brain, especially in the hippocampus. This can cause the persistent learning/memory deficits later on life. This study examined whether pentobarbital, an anesthetic with GABAergic property, administered to neonate rats, can trigger the behavioral and electrophysiological deficits occur later in adulthood. Rats administered pentobarbital (10 and 20 mg/kg, i.p.) on the 7th day after birth (7PD) displayed suppressed the hippocampal long-term potentiation (LTP) at 10-12 weeks old. Paired-pulse facilitation was augmented by pentobarbital, suggesting the presynaptic depression in the hippocampus. The behavioral exploration, tested by the open field test, showed the tendency of suppression. Exploration in the open-field test has shown to correlate to the hippocampal function, i.e. spatial memory and learning. These data suggest that administration of pentobarbital during a critical stage of brain development may result in functional deficits of hippocampus in adulthood. On the other hand, blood gas analysis during the pentobarbital anesthesia at 7PD induced the critical hypoxia and/or systemic acidosis via the respiratory depression. Given that neonatal hypoxia and/or systemic acidosis can cause the hippocampal dysfunction later on life, we have to take that bias into consideration when discussing the functional deficits induced by pentobarbital during a critical stage of neonatal brain development.