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The effects on phrenic nerve discharge elicited by intraspinal stimulation which produced synchronous activation of bulbo-spinal inspiratory neurones were investigated in chloralose-urethane anaesthetized, paralysed, vagotomized and artificially ventilated cats. Descending respiratory axons were activated in the ventrolateral spinal cord at the second cervical level using either monopolar or bipolar stimulation (25-200 microA, 100 microseconds, 1-300 Hz). Activation of bulbo-spinal axons was confirmed by recording both orthodromic phrenic nerve excitation and antidromic spike invasion of single, inspiratory modulated units in either the dorsal respiratory group (d.r.g.) or ventral respiratory group (v.r.g.). Antidromic activation of inspiratory bulbo-spinal neurones was confirmed by the criteria of high frequency following and collision tests. Spinal cord stimulation at intensities of 100 microA antidromically activated approximately half of the inspiratory bulbo-spinal neurones in the d.r.g. and v.r.g. Stimulation pulses delivered to the spinal cord elicited an orthodromic excitation of the ipsilateral phrenic nerve lasting 2-12 ms during inspiration. The onset latency of excitation was 2-4 ms, decreasing as inspiration progressed. Following the initial excitation there was a 4-30 ms period of reduced phrenic nerve discharge. Continuous trains of stimuli (less than 100 microA, 100 microseconds, 1-300 Hz) or phrenic gated trains delivered during every fourth inspiratory or expiratory cycle had little or no effect on the duration of inspiration or expiration. Brief trains (400 ms, 50 Hz, 100 microA) of bilateral spinal cord stimulation delivered at various delays from the onset of inspiration had only a transient effect on the pattern of phrenic nerve discharge, with no noticeable effect 60 ms after termination of stimulation. Based on the assumption that synchronous activation of a portion of the central pattern generator for respiration would phase shift or reset the rhythm, we conclude that the bulbo-spinal inspiratory neurones are not responsible for generation of respiratory timing signals and play, at most, a limited role in the generation of the augmenting central inspiratory activity.

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