Immunohistochemical estimation of rat spinal somatostatin in the antinociceptive response induced by thiamine deficiency

The mechanism of the antinociceptive effect induced by thiamine deficiency (TD) was examined. Pain threshold as measured by the hot-plate test increas ed gradually within days after the start of TD diet. The antinociceptive ef fect was significantly increased in proportion to the decreased somatostati n fluorescence intensity in the spinal cord. A single injection of thiamine HCl (0.5 mg/rat, s.c.) on the 14th day of the TD diet reversed the pain th reshold as evaluated by hot-plate test to nearly control levels. Whereas, t his reversal effect was not observed if the thiamine HCl treatment was done relatively later. When thiamine HCl was injected on a day early in the die t, the fluorescence intensity of somatostatin in the spinal cord remained a lmost the same as the normal diet group. These results indicated that the a ntinociceptive effects induced by TD are the result of a marked degeneratio n of the primary afferent neuron or the somatostatin concentration in the s pinal dorsal horn.