Short-term depression of inspiratory activity following tonic vagal stimulation.

This study tested the role of inhibitory neurotransmission in the glutaminergic control of short-term depression (STD) of the inspiratory activity initiated by sustained stimulation of the vagus nerve in anesthetized and vagotomized cats. STD, calculated from the integrated phrenic nerve signal, lasted longer when glutaminergic neurotransmission was inhibited by ketamine, a NMDA receptor antagonist. Application of picrotoxin, a GABAA receptor antagonist, reversed the effect of ketamine and shortened the STD duration below that present in the control condition. The results showed that alternation of the neural excitability by antagonists of excitatory and inhibitory neurotransmission modulates the STD of inspiratory activity, evoked by vagal stimulation. The STD depends on the state of neural excitability and is easier accomplished when the excitability is on the high side.