SUMMARY1. Reflexes to sacral parasympathetic neurones were studied by electrophysiological techniques in decerebrate, in chloralose-anaesthetized, and in chronic spinal cats.2. Excitatory reflexes from pelvic nerve and sacral somatic afferent nerve fibres were present before and after chronic transection of the spinal cord, but the latencies differed markedly. It was concluded that the longlatency reflexes observed when the spinal cord was intact involved longloop reflexes to the brain-stem. The weak, short-latency reflexes in the chronic spinal cat were never observed when the spinal cord was intact and could be due to reorganized spinal connexions. The short-latency reflexes are probably unimportant in normal micturition.3. Stimulation of afferent fibres in the pelvic or sacral somatic nerves produced short-latency inhibitory post-synaptic potentials (IPSPs) and inhibition of discharges in parasympathetic neurones. This inhibition was due to a spinal reflex. 4. A local reflex was demonstrated in the pelvic plexus. This was probably a cholinergic axon reflex, but the remote possibility that it was a local cholinergic reflex involving sensory neurones in the bladder wall has not been excluded.

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SUMMARY1. The effects produced by stimulation of the central end of transected ventral roots were observed on spontaneous and evoked vesical contractions and on the firing of sacral parasympathetic neurones.2. Recurrent inhibition of sacral parasympathetic neurones was demonstrated at frequencies of stimulation above 10/sec and at intensities above threshold for the parasympathetic axons.3. Recurrent inhibition was present in chloralose cats, as well as in decerebrate animals and was unaffected by chronic spinal transection.4. Interneurones were located which are presumed to be the autonomic equivalents of the somatic Renshaw cells. They were synaptically activated by antidromic stimulation of preganglionic fibres in sacral ventral roots.5. The inhibition of vesical contractions and the firing of the interneurones was reduced when the intravesical pressure was raised.6. The recurrent inhibition was unaffected by the intravenous injection of dihydro-,8-erythroidine.7. Strychnine reduced the recurrent inhibition in some experiments but the results were inconsistent. The effects of picrotoxin were inconclusive. 8. The possible role of recurrent inhibition in micturition is discussed.

SUMMARY1. The effect of electrical stimulation of the brain stem on reflex transmission has been investigated in decerebrate cats after partial transection of the spinal cord.2. Brain stem stimuli that do not evoke inhibitory post-synaptic potentials (IPSPs) in motoneurones or primary afferent depolarization may still effectively depress the excitatory and inhibitory synaptic actions evoked from the flexor reflex afferents (FRA) and from lb afferents. There is no effect on post-synaptic potentials from Ia afferents or on Renshaw IPSPs. The depression is not associated with any measurable change in conductance over the motoneuronal membrane.3. There is also inhibition from the brain stem of transmission from the FRA (but not from Ia and Ib afferents) to primary afferqnt terminals and to ascending spinal pathways. 4. It is concluded that this inhibition from the brain stem is exerted at an interneuronal level in spinal reflex paths.5. The inhibitory action is evoked from the region ofMagoun's inhibitory centres in the brain stem and is mediated by axons with a conduction velocity of at least 20 m/sec. The axons are distributed in the dorsal part of the lateral funicle.6. The pathway mediating the inhibition from the brain stem is named the dorsal reticulospinal system. Its possible role in maintaining the decerebrate control of reflexes is discussed and related to the problem of a selective control of some paths from a primary afferent system.

SUMMARY1. L-Noradrenaline (NA), 5-hydroxytryptamine (5-HT) and acetylcholine (ACh) were administered micro-electrophoretically to feline lumbar neurones while recording their spike potentials extracellularly.2. There was no evidence to suggest that NA acts as an excitatory transmitter in the spinal cord.3. NA had potent inhibitory effects on some interneurones as revealed by a depression of spontaneous and synaptic firing and on the firing to a local application of an excitant amino acid. The effects on Renshaw cells and motoneurones were less marked.4. The depressant actions of 5-HT were less marked than those of NA. ACh and carbamylcholine had depressant effects on some NA-sensitive interneurones but were invariably far less potent and on other NA-sensitive cells were completely inactive.5. NA had no detectable effect on the normal spike amplitude but when the action potentials were reduced by excessive depolarization then both NA and synaptic inhibition increased the spike amplitude; this effect could be due to a hyperpolarization of the cell membrane.6. There was a correlation between the distribution of NA-sensitive cells and the relative densities of NA-containing terminals in various layers of the grey matter.7. It was postulated that NA acts as an inhibitory transmitter released from the terminals of descending pathways in the spinal cord. Other possible mechanisms were discussed but lacked experimental support.

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