Investigations in the past decade indicate that functional bowel disorders, for example, irritable bowel syndrome (IBS), involve hypersensitivity (hyperalgesia) and hyper-reflexia of the gut. Thus seemingly normal patients suffer pain and discomfort during digestion, and sometimes have exaggerated enteric reflexes.1-3

We have recently discovered a phenomenon that may be related to intestinal hypersensitivity and hyper-reflexia, sustained slow postsynaptic excitation (SSPE), which occurs in intrinsic sensory neurones of the small intestine.4 SSPE can be evoked by moderate stimulation of presynaptic inputs to intrinsic sensory neurones (AH neurones) in the small intestine and results in substantially enhanced excitability of these neurones that can outlast stimulation by several hours. It is possible that SSPE is involved in changed intestinal function, following alterations in alimentary activity, and in the genesis of functional bowel disorders. To our knowledge, there is no other documented long term change in the responsiveness of enteric neurones and thus no other candidate mechanism for inducing hyper-reactivity within the enteric nervous system.