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Review
. 2009 Dec;111(6):1365-71.
doi: 10.1097/ALN.0b013e3181bf1d61.

Neurotoxicity of general anesthetics: cause for concern?

Misha Perouansky  1 , Hugh C Hemmings Jr
Affiliations
Review

Neurotoxicity of general anesthetics: cause for concern?

Misha Perouansky et al. Anesthesiology. 2009 Dec.
No abstract available

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Figures

Fig. 1
Fig. 1. Developmental vulnerability to neurotoxicity due to paradoxical GABAergic excitation
Animal models have provided convincing evidence for drug-induced apoptotic neurodegeneration. The peaks of vulnerability to early (E19) and late (P7) apoptotic neurodegeneration induced by ethanol in rat brain are indicated. The development of rat brain compared to that of the macaque is shown in the lower axes with approximate corresponding developmental milestones. Neurogenesis occurs before E80 in primate, which corresponds to birth in rat. A single day in rat neurodevelopment (P7) translates to 32 days in the primate. Note that axons develop before dendrites and spines, and GABA synapses before glutamate synapses. Excitotoxicty resulting from GABAA-enhancing anesthetics is considered a plausible model for neurodegeneration. During development, GABA changes from excitatory (depolarizing) to inhibitory (hyperpolarizing) because the intracellular chloride concentration decreases due to changes in the expression of the two major chloride cotransporters, KCC2 and NKCC1 that are differentially expressed during development. Paradoxical excitation of immature neurons by activation of GABAA receptors generates an efflux of chloride and excitation in immature neurons (left inset), in contrast to the influx of chloride with inhibition in mature neurons (right inset.
See this image and copyright information in PMC

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