Modulation of afferent nerve activity by prostaglandin E2 upon urinary bladder distension in rats.

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What is the central question of this study? It has been widely assumed that Cfibres innervating the bladder are mainly excited in overactive bladder syndrome. However, it remains unclear whether Aδ fibres are also activated in pathological conditions. What is the main finding and its importance? We found that a certain population of Aδ fibres, which become active specifically at a bladder pressure of more than 15cmH2 O in normal conditions, showed increased excitability in conditions of prostaglandin E2 -induced overactive bladder. This result suggests that a certain population of Aδ fibres, together with Cfibres, triggers pathophysiological activity. In overactive bladder syndrome, afferent Cfibres innervating the bladder show an increased activity level. However, it remains unclear whether all Cfibres are highly activated and whether Aδ fibres, the other type of bladder afferent fibre, are also involved in pathological conditions. To address these questions, we analysed the relationship between bladder pressure and single-unit firing patterns of afferent nerves in the left L6 dorsal roots in living rats. The recorded fibres were classified as Aδ fibres or Cfibres based on the response to 0.3μm tetrodotoxin. Certain populations of both Aδ fibres and Cfibres were activated at bladder pressures below 15cmH2 O (classified as low-threshold fibres), indicating their potential contribution to detection of normal bladder filling. Intravesical administration of prostaglandinE2 (PGE2 ) induced hyperexcitation in approximately half of such Cfibres, whereas the activity patterns of low-threshold Aδ fibres were unchanged. All fibres, regardless of type, which were almost silent in control conditions (classified as high-threshold fibres), were activated by application of PGE2 . Notably, the firing patterns of Aδ fibres, rather than Cfibres, were highly time locked to PGE2 -induced micro-oscillation of bladder pressure. These modulatory effects of PGE2 on Aδ fibres and Cfibres might trigger pathophysiological activity together in overactive bladder syndrome.