Ashley Rebecca Miles, Peter John Hawrysh, Nariman Hossein-Javaheri, and Leslie Thomas Buck

Unlike anoxia-intolerant mammals, painted turtles can survive extended periods without oxygen. This is partly accomplished by an anoxia-mediated increase in gamma-aminobutyric acid (GABA) release, which activates GABA receptors and mediates spike arrest in turtle neurons via shunting inhibition. Extracellular taurine levels also increase during anoxia; however, its function is unknown but speculated to involve glycine and/or GABAA/B receptors. Given the general importance of inhibitory neurotransmission in the anoxia-tolerant painted turtle brain, we investigated the function of taurine as an inhibitory neuromodulator in turtle pyramidal neurons. Using whole-cell patch-clamp electrophysiological methods to record from neurons within a cortical brain sheet, we found that taurine depolarized membrane potential by approximately 8 mV, increased whole cell conductance by approximately 2-fold, and induced an inward current that possessed characteristics similar to GABA- and glycine-evoked currents. These effects were mitigated following glycine receptor antagonism with strychnine and GABAA receptor antagonism with gabazine, bicuculine, or picrotoxin, but were unchanged following GABAB or glutamatergic receptor inhibition. These data indicate that high concentrations of taurine in vitro mediates its effects through both glycine and GABAA receptors, and suggest that taurine, in addition to GABA, inhibits neuronal activity during anoxia in the turtle cortex.

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