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Department of Physiology, Royal Free Hospital School of Medicine, London.

1. Intracellular recordings were made from caudal medullary expiratory neurones in anaesthetized, paralysed, artificially ventilated and vagotomized cats before during and after the tachypnoeic response evoked by stimulation of the perifornical region of the hypothalamus. 2. The tachypnoeic response was evoked in seven of ten cats tested, and was represented in the phrenic nerve by a rapid two- to threefold increase in the frequency of the respiratory rhythm. The shortened duration of inspiratory discharge in the phrenic nerve was accompanied by an increase in its rate of development. If initially present, post-inspiratory phrenic discharge was intensified and extended throughout the shortened expiratory interval. 3. Intracellular recordings were obtained from twenty-one expiratory neurones during intermittent hypothalamic stimulation with short trains of pulses. Eighteen neurones showed a regular, short-latency sequence of synaptic events which consisted of an initial depolarizing potential (presumed EPSP) and a following hyperpolarizing potential (Cl--mediated IPSP) of long duration (50-150 ms when measured in expiration). The IPSP was accompanied by a phasic cessation of phrenic nerve discharge of comparable duration which was succeeded by intensified discharge. In three neurones (one experiment) the IPSP response was absent. 4. Sixteen neurones showing the EPSP-IPSP sequence were held for sufficiently long to record changes in the respiratory-related membrane potential pattern accompanying stimulation. The reduced expiratory time accompanying the response resulted in a shortened expiratory burst. In four neurones showing evidence of IPSPs in early expiration (post-inspiratory IPSPs), stimulation resulted in a phasic weakening of this inhibition which resulted in a more rapid approach to threshold and a steady rather than delayed increase in discharge. A low level of post-inspiratory IPSPs extended throughout most of the shortened expiration, resulting in an alternating rhythm of inspiratory and post-inspiratory inhibition. In the twelve neurones lacking such post-inspiratory IPSPs stimulation had no obvious effect on the shape of the expiratory trajectory. 5. In neurones which received an IPSP from hypothalamic stimulation, the overall response was associated with reduced amplitude and increased rate of decline of inspiratory inhibition of expiratory neurones. Three neurones showed high-frequency (70-80 Hz) oscillation of the membrane potential during inspiration (Mitchell & Herbert, 1974b). Hypothalamic stimulation resulted in a transient suppression of this oscillation. 6. We conclude that the short-latency inhibitory component of the response to hypothalamic stimulation is widely distributed, including expiratory neurones, some fraction of the inspiratory population and the neurones responsible for inspiratory and post-inspiratory inhibition.