Fig. 3. During inspiratory bursts, the average frequency of glycinergic synaptic inputs to cardiac vagal neurons (CVNs) significantly increased during inspiratory activity (  left ). Ketamine suppressed the increase in glycinergic frequency during inspiration at a dose of 0.5 μm (  middle ) and further reduced the inspiratory-evoked increase in glycinergic neurotransmission during inspiration at 1 μm (  right ). The inhibitory action of ketamine on glycinergic neurotransmission to CVNs during inspiration was reversible, and all inhibitory postsynaptic currents (IPSCs) under these recording conditions were blocked by the application of the glycine antagonist strychnine (1 μm).