News and Events

Anesthesia-induced neurotoxicity may cause permanent dysfunctions in human brains. In this work, we used a cell-based in-vitro model to demonstrate that traditional Chinese medicine, Kami-Shoyo-San may protect ketamine-induced neuronal apoptosis in human embryonic stem cell-differentiated neurons.

A large number of preclinical studies have established that general anesthetics (GAs) may cause neurodevelopmental toxicity in rodents and nonhuman primates, which is followed by long-term cognitive deficits. The subiculum, the main output structure of hippocampal formation, is one of the brain regions most sensitive to exposure to GAs at the peak of synaptogenesis (i.e., postnatal day (PND) 7). We have previously shown that subicular neurons exposed to GAs produce excessive amounts of reactive oxygen species (ROS), such as hydrogen peroxide (H₂O₂), which is a known modulator of neuronal excitability.

The cation-chloride cotransporters Na⁺-K⁺-2Cl^–-1 (NKCC1) and K⁺-2Cl^–-2 (KCC2) critically regulate neuronal responses to gamma-aminobutyric acid (GABA). NKCC1 renders GABA excitatory in immature neurons while expression of KCC2 signals GABA maturation to its inhibitory role. Imbalances in NKCC1/KCC2 alter GABA neurotransmission, which may contribute to hyperexcitability and blunted inhibition in neurocircuitry after neonatal exposure to anesthesia. Thus, we hypothesized that anesthetics may dysregulate NKCC1 and/or KCC2 in developing brain.

Several animal and emerging human studies suggest an association between an early exposure to general anesthesia (GA) and long-lasting problems with complex social and emotional behaviors such as inattentiveness, impulsivity, anxiogenic tendencies, as well as difficulties engaging in proper social intercourse, with significant increase in attention deficit and hyperactivity-type behaviors. To further investigate these behaviors, and to examine the potential of presently available rodent behavioral models to guide future assessments of long-term socio-emotional impairments in humans, we examined the long-term effects of GA on anxiety/fear and social behaviors.

General anesthesia (GA) is usually considered to safely induce a reversible unconscious state allowing surgery to be performed without pain. A growing number of studies, in particular pre-clinical studies, however, demonstrate that general anesthetics can cause neuronal death and even long-term neurological deficits. Herein, we report our literature review and meta-analysis data of the neurological outcomes after anesthesia in the young.

Millions of babies and children undergo anaesthesia every year. Preclinical evidence shows that all common anaesthetic drugs are associated with neuro-apoptosis and neurodevelopmental deficits in immature rodent models. Xenon, a low-potency anaesthetic gas, renowned for producing cardiostable anaesthesia and with neuroprotective properties in multiple pathologies, was recently used to reduce sevoflurane requirements of babies and young children undergoing cardiac catheterisation.