Fig. 3.

Removal of PSA from the spinal cord exacerbates thermal hyperalgesia and reduces C-fiber atrophy. (A) Graph representing tolerance to thermal stimuli as assessed by hindpaw withdrawal in the hot-plate test. Sciatic ligation alone shortens the latency of withdrawal. Removal of PSA by endo N significantly (P < 0.01) and persistently intensifies this hyperalgesia. W, week; B, graph showing the CCI-induced loss of lamina II C terminals. The density of TMP staining in lamina II was quantified (see Materials and Methods), and the ratio of the density on the ligated side to that on the unligated side was calculated. The CCI-induced loss of TMP staining was then expressed as percentage of that obtained in vehicle-treated samples. The loss of C terminals is maximal in the presence of PSA (Vehicle). The absence of this carbohydrate from the tissue significantly reduces (47.5% ± 9.7; P < 0.01) the C-terminal loss in lamina II (endo N). (C) Spinal cross sections processed for TMP histoenzymology, a specific staining for C terminals. Note the normal staining pattern in lamina II of the control unligated side. A marked reduction in lamina II TMP staining is induced by ligation in the presence of PSA in the vehicle-treated group (arrows). Removal of PSA by endo N results in the preservation of more terminals. (Bar, 150 μm.)