Suppression of spike amplitudes in the hippocampus up to 40 min after stimulation is seen in adult rats when exposed to sevoflurane as an infant. (Image source: Thinkstock)

Suppression of spike amplitudes in the hippocampus up to 40 min after stimulation is seen in adult rats when exposed to sevoflurane as an infant. (Image source: Thinkstock)

Animal studies are convincing: when newborn animals are exposed to anesthesia, neuroapoptosis, or neural cell death, develops. Cell death is associated with learning disabilities. Hippocampal synaptic plasticity is known to affect learning and memory. Dr. Rui Kato, Department of Anesthesiology and Critical Care Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan, and colleagues sought to determine whether exposure to 1% or 2% sevoflurane for 2 hours impaired the hippocampal synaptic plasticity of postnatal day 7 rat pups. Their work, titled “Neonatal Exposure to Sevoflurane Causes Significant Suppression of Hippocampal Long-Term Potentiation in Postgrowth Rats,” is published in this month’s issue of Anesthesia & Analgesia.

The rat pups were exposed to either 1% or 2% sevoflurane for 2 hours. Then, between postnatal days 63 & 70, i.e., as adults, and while anesthetized with halothane 1%, they were placed in a stereotactic apparatus, a recording electrode was placed in the hippocampal CA1 region, and a stimulating electrode was placed in ipsilateral Schaffer collaterals. A stimulus resulted in activation of pyramidal cells of the CA1 region.

Neonatal exposure to 2% sevoflurane resulted in suppression of long-term potentiation induction in adults up to 40 minutes after high-frequency stimulation.

Changes in synaptic plasticity following sevoflurane exposure may be one reason why neurocognitive dysfunction occurs. It will be interesting to see if measures that ameliorate cognitive dysfunction may be associated with reversal of this suppression.