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1. Electrophysiological and micro‐electrophoretic studies were carried out in anaesthetized cats on spinal interneurones which were monosynaptically activated from group 1 muscle afferents and recurrently inhibited by Renshaw cells. 2. The recurrent inhibition was blocked by the iontophoretic administration of strychnine, which also blocked the action of glycine. 3. The time course of the block of synaptic inhibition by strychnine was slower than the block of glycine evoked inhibition. The significance of this observation in terms of the location of the inhibitory synapses is discussed. 4. The observation that recurrent inhibition of motoneurones and of interneurones is blocked by strychnine whereas the mutual inhibition of Renshaw cells is not is discussed in relation to the proposal that the nature of the post‐synaptic inhibitory receptor is not determined solely by the innervating neurone, which is the Renshaw cell in all three instances. 5. The recurrent inhibition of the interneurones was not blocked by the iontophoretic administration of bicuculline, but difficulties were encountered in demonstrating that this agent consistently antagonized the inhibitory effects of GABA.

1. Extracellular recordings of postsynaptic potentials (field potentials), population spikes or unitary action potentials and intracellular records of excitatory and inhibitory postsynaptic potentials were obtained from neurons in superfused slices of rat hippocampus, to study the mechanism of the excitatory effect of enkephalins. 2. Most experiments were carried out with a synthetic, stable enkephalin analogue (FK 33‐824) administered either by perfusion or by local administration (ionophoresis or pressure application from micropipettes). Comparisons were made when appropriate with metenkephalin, morphine, 4‐aminopyridine and bicuculline. 3. The enkephalins caused a small increase in extracellular recordings of e.p.s.p.s and a more marked increase in the amplitude and frequency of population spikes. The effect of 4‐aminopyridine on the extracellular e.p.s.p. was more marked than that of enkephalins, indicating that the enkephalins may have an additional effect upon regenerative spike mechanisms in the dendrites, which is not possessed by 4‐aminopyridine. The actions of the enkephalins and morphine were blocked by naloxone, which did not block the action of bicuculline or 4‐aminopyridine. 4. The increase in extracellularly recorded e.p.s.p. was shown to be due to a marked increase in the e.p.s.p. amplitude recorded intracellularly in CA1 and CA3 neurones and dentate granule cells. The augmented e.p.s.p.s evoked more action potentials. 5. The increase in e.p.s.p. amplitude was not accompanied by any marked change in membrane potential or resistance. 6. The inhibition of background firing by appropriate stimulation and recorded as peristimulus histograms was not reduced by FK 33‐824. There was a slight prolongation. 7. Intracellularly recorded i.p.s.p.s were not blocked by FK 33‐824. There was a prolongation of the i.p.s.p.s and an apparent increase in latency due to the unmasking and prolongation of e.p.s.p.s. 8. Dendritic excitability, as tested with ionophoresis of DL‐homocysteic acid locally to the dendrites was unaffected by FK 33‐824. 9. It is concluded that the increase in e.p.s.p.s produced by enkephalins can be explained by an increased release of excitatory transmitter, as occurs with 4‐aminopyridine.

1. Patterns of convergent excitation and mutual inhibition of Renshaw cells to antidromic volleys in motor axons were investigated in cats anaesthetized with chloralose. 2. There were widely varying patterns of excitatory convergence onto individual Renshaw cells, but grouping the cells into different populations revealed the underlying positive and negative correlations between inputs from different motor nerves. 3. The greatest excitatory convergence was seen between axons supplying functionally synergistic muscles. 4. Mutual inhibition between Renshaw cell populations was most evident between antagonist motoneurones and so was inversely related to the excitatory inputs. 5. These results are discussed in relation to the control of recurrent inhibitory phenomena mediated by renshaw cells.

1. The actions of microelectrophoretically administered substance P on Renshaw cells in pentobarbitone anaesthetized cats were investigated. 2. The effects on spontaneous and synaptic firing and interactions with a number of other agents including acetylcholine, acetyl‐beta‐methylcholine, acidic amino acids, morphine, dihydro‐beta‐erythroidine and strychnine were studied in attempts to elucidate the mechanism of action of substance P. 3. Substance P usually selectively depressed the excitation by ACh, and also reduced submaximal synaptically evoked discharges which activate nicotinic receptors, but failed to modify excitation caused either by acetyl‐beta‐methylcholine, which activates muscarinic receptors, or excitation caused by glutamate or homocysteate. Substance P also depressed excitation by morphine which acted via the nicotinic receptors. 4. The inhibitory effect was not blocked by strychinine and was considered to be unlikely to be due to interaction between the polypeptide and either glycine or GABA receptors. 5. On some cells substance P caused excitation which was blocked by dihydro‐beta‐erythroidine. Mixed excitatory‐inhibitory effects were observed on some of these neurones. 6. The results are discussed in relation to the possibility that substance P could function as a synaptic inhibitory mediator with an unusual selectivity of action.

Preganglionic neurones in the fourth thoracic segment of anaesthetized cats fired spontaneously at a rate of about 2/sec. The effects of micro-electrophoretic administration of 5-hydroxytryptamine, noradrenaline, acetylcholine and DL-homocysteic acid on this spontaneous firing were determined. Many cells were excited by 5-hydroxytryptamine (5HT) and DL-homocysteic acid (DLH), a few were depressed by noradrenaline (NAdr), but acetylcholine (ACh) was inactive. The data are consistent with the view that 5HT and NAdr may function as excitatory and inhibitory transmitters which are released from the terminals of descending pathways in the spinal cord.

1. Sacral parasympathetic preganglionic neurones were identified by intracellular and extracellular micro‐electrode recording of antidromic potentials in response to stimulation of the pelvic nerve or the second or third sacral ventral roots.

1. 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.

1. 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.

1. The effect of electrical stimulation of the brain stem on interneurones in the dorsal horn and intermediary region has been investigated in decerebrate cats after partial transection of the spinal cord.

1. Reflexes to sacral parasympathetic neurones were studied by electrophysiological techniques in decerebrate, in chloralose‐anaesthetized, and in chronic spinal cats.

1. L‐Noradrenaline (NA), 5‐hydroxytryptamine (5‐HT) and acetylcholine (ACh) were administered micro‐electrophoretically to feline lumbar neurones while recording their spike potentials extracellularly.