1. Repetitive stimulation of guinea‐pig hypogastric nerves elicited, in addition to the fast cholinergic excitatory potential, a slow depolarization lasting for seconds to minutes in neurones of the isolated inferior mesenteric ganglion. 2. The slow depolarization which could be elicited at a frequency as low as 1‐2 Hz for several seconds was not blocked by cholinergic antagonists, but was eliminated in a low Ca2+ solution; it was termed henceforth the non‐cholinergic excitatory potential. 3. When the membrane potential was manually clamped, the non‐cholinergic potential was associated with three types of membrane resistance change: an increase, a delayed increase and a biphasic change consisting of an initial decrease followed by an increase. 4. In the majority of neurones, conditioning hyperpolarization augmented the non‐cholinergic depolarization; in a few neurones, moderate hyperpolarization depressed the latter, whereas stronger hyperpolarization unmasked a low depolarization. 5. The non‐cholinergic response was markedly attenuated in the presence of exogenously applied substance P; it was partially suppressed by luteinizing hormone‐releasing hormone. 6. Non‐cholinergic depolarization could be elicited in the same neurone by stimulation of all four nerve trunks associated with the ganglion. 7. It is suggested that substance P, a peptide, may be the transmitter responsible for the generation of the non‐cholinergic potential and that it may be released from collateral endings of primary sensory neurones, thus providing a functional connexion between sensory and autonomic neurones.
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