Fig. 6. Summary scheme of the effect of 1 minimum alveolar concentration (MAC) halothane and sevoflurane on synaptic transmission to expiratory premotor neurons in the caudal ventral respiratory group. The overall glutamatergic excitatory drive is reduced (↓) without change in N -methyl-d-aspartate (NMDA) receptor activity (Ø2,5). Overall inhibition is increased (↑) as a result of a strong increase (↑) in γ-aminobutyric acid type A (GABA^A) receptor function, whereas presynaptic inhibitory drive appears reduced. The combined effects lead to a decrease in control discharge frequency (F^con) of the premotor neuron.