Abstract

Intracellular recording methods were used to examine stereotyped reflexes evoked in the circular muscle of guinea-pig small intestine by distension or repetitive deformation of the mucosal villi, in vitro. Both stimuli evoked compound excitatory junction potentials (EJPs) on the oral side of the site of stimulation and compound inhibitory junction potentials (IJPs) on the anal side. Stimulation of the mucosa by application of 10 μl of 0.5 M HCl evoked similar reflex responses in the circular muscle. The compound EJPs evoked by mucosal stimulation were depressed, but not abolished, by 1 μM hyoscine, indicating that these responses were partially mediated by release of acetylcholine, as are the equivalent responses evoked by distension. The compound EJPs and the compound IJPs evoked by maintained distension or by repeated mechanical stimulation of the mucosa were transient, lasting in most cases for 3–5 s before the membrane potential returned to resting level. This decline (rundown) occurred in part of the circuit close to the site of stimulation as stimuli applied elsewhere during the period of rundown evoked normal EJPs and IJPs. Mechanical stimuli (brush strokes that deformed the mucosal villi) applied to the mucosa at the site of a maintained distension evoked responses of normal amplitude during the period when the response to the distension had declined to zero. In contrast, during the period when the responses to repetitive mechanical stimulation of the mucosa had disappeared, the reflex responses evoked by distension at the same site were substantially augmented. Chemical stimulation of the mucosa with acid also enhanced the responses to distension. These enhancements were observed even though direct responses to mucosal stimulation could no longer be observed. It is concluded that distension evoked reflexes and reflexes evoked by mucosal stimulation are mediated by separate populations of sensory neurons. The results also indicate that sensory stimulation of the mucosa activates a pathway that interacts with the distension reflex pathway to enhance its activity, but has no maintained direct effect on the circular muscle itself.

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