γ-Aminobutyric Acid

Although rats administered 1% to 4% atm halothane for 30 minutes exhibit no change in whole-brain GABA content,^[67] anesthesia may alter GABA levels in selected regions of the brain. Treatment of rat cerebral cortex slices with 3% atm halothane inhibits the metabolism and increases the content of the inhibitory transmitter GABA but does not affect the uptake or release of GABA.^[68] If the accumulation of GABA in inhibitory neurons is associated with an increase in inhibitory activity, the resulting decrease in synaptic transmission may contribute to the anesthetic state. ^[68] Consistent with this hypothesis is the reversal of isoflurane-induced suppression of thalamocortical relay neurons by the local iontophoretic application of a GABA_A -receptor antagonist^[69] and the ability of GABA_A -receptor antagonists to increase the isoflurane MAC in rats.^{[70] [71]}