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The respiratory modulation of the activity of vagal cardio-inhibitory neurones of the nucleus ambiguus of the cat has been investigated by electrophysiological and neuropharmacological techniques. All twenty-four vagal efferent neurones studied had axons with conduction velocities indicative of B fibres and projected to the right cardiac branches of the vagus. Their spontaneous or DL-homocysteic acid (DLH)-evoked activity showed a marked reduction during the phase of inspiration and all showed signs of receiving a baroreceptor input. Ionophoretic application of DLH always excited cardiac vagal motoneurones (c.v.m.s). Application of acetylcholine to these same cells provoked a decrease in firing rate in twelve of the fifteen neurones tested. In ten of these twelve cells simultaneous application of atropine antagonized the effect of acetylcholine. Atropine applied alone enhanced neuronal firing, particularly in inspiration. Stable intracellular recordings have been made from two c.v.m.s. These were inhibited during inspiration. Input resistance fell markedly during inspiration and injection of chloride reversed this wave of hyperpolarization to a wave of depolarization indicating that this resulted from chloride-mediated inhibitory post-synaptic potentials (i.p.s.p.s). These c.v.m.s were activated during Stage I expiration, and showed a weak and variable wave of inhibition in Stage II expiration. Pulse-rhythmic depolarizing potentials were reduced in their amplitudes during the periods of decreased neurone input resistance. It is concluded that c.v.m.s receive an excitatory input during post-inspiration and a powerful inhibitory synaptic input during inspiration. The implications of these observations for the physiology of cardiorespiratory reflexes are discussed.
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