The present study was undertaken to investigate modification in electrophysiological characteristics of cat dorsal horn cells resulting from carrageenin-induced inflammation. The followings were studied; 1) the time-course of changes in responses of the WDR (wide dynamic range) cell 1-3h after subcutaneous injection of carrageenin in its receptive field; 2) the responses of the same dorsal hern cells before and after induction of inflammation; 3) the effect of inflammation on the responsiveness of dorsal horn neurons to algogens (bradykinin & potassium); and 4) the effect of inflammation on the activity of WDR cell following administration of indomethacin and clonidine. Though responses of WDR neuron were increased dramatically during first 1h, the maximal enhancement was observed 3h after induction of inflammation especially by repetitive light tactile stimulus. Following carrageenin injection the majority of WDR neurons (10/15 units) showed enhanced responses to all the mechanical stimuli while in 3 cases responsiveness were intensified during activation by one tactile stimulus (brush or pressure). One cell was unaffected by inflammation and in another case the response was enhanced only to noxious stimulus. Five of 9 cells that could initially be driven by noxious stimulus were activated more strongly by same stimulus and even by tactile stimulus (pressure) following inflammation. In 2 cases neurons were sensitized only to noxious stimulus whereas in another 2 cells that did not show enhanced responses to noxious stimulus responses to light tactile stimulus (pressure) appeared after inflammation. Of 16 LT cells tested 6 responded to squeeze while 4 showed the characteristics of WDR cell following inflammation. No modification in responsiveness was recognized in 3 cells whereas response to only brush was enhanced in another 3 neurons. Following carrageenin injection responses of LT cell to bradykinin or K⁺ were not altered whereas those of WOR neurons to bradykinin or K⁺ were suppressed in 22.2% and 33.3% of cases, respectively. In two of 8 activity of HT cells were inhibited by bradykinin while in five of 8 responsiveness to K⁺ were rather enhanced by inflammation. In the rest inflammation was ineffective. In inflammation-induced animal the receptive field of LT cell was not changed whereas those of WDR cell and HT cell were tremendously expanded. The enhanced responses of WDR neurons to mechanical stimuli resulted from inflammation were suppressed by intravenously injected indomethacin and clonidine suggesting that postaglandin is involved in inflammation-induced sensitization of these cells. The involvement of peripheral and central mechanisms in the modification in responsiveness of dorsal horn cells in the carrageenin-induced inflammation was discussed.