TY - JOUR
T1 - Properties of high-threshold mechanoreceptors in the goat oral mucosa. II. Dynamic and static reactivity in carrageenan-inflamed mucosa
AU - Cooper, B.
AU - Ahlquist, M.
AU - Friedman, R. M.
AU - Labanc, J.
PY - 1991
Y1 - 1991
N2 - 1. We have previously described two classes of high-threshold mechanoreceptors (HTMs) of the oral mucosa of the goat. Mechanonociceptors (MNs) had very high thresholds (16-300 g) and were poor transducers of pressure. Intense pressure receptors (IPRs) had thresholds from 2 to 16 g and were good transducers of pressure. After carrageenan inflammation (CI) we observed mechanical sensitization in both classes of HTMs. The characteristics were as follows. 2. Sensitization of MNs was manifested as qualitative shifts in the capacity to encode intense pressure. MNs that were unable to code intensity before CI acquired pressure coding properties after treatment with carrageenan. Qualitative shifts in coding capacity were suggested by the greater proportion of MNs coding in preinflamed (10 of 14) compared with noninflamed tissue (8 of 25 cases). Improved afferent reactivity was directly observed, in additional experiments, in which MNs were characterized in normal tissue before the injection of carrageenan into the mucosa. In five of six cases, either qualitative or quantitative improvements were observed. In control experiments, improved reactivity was observed in one of six cases. 3. Sensitization in IPRs was manifested as both qualitative and quantitative improvement in intensity coding properties. Power functions fit to individual IPRs indicated sensitization for most mucosal afferents after inflammation. Carrageenan induced decreases in the mean response interval, pressure-frequency threshold (PFT), and pressure-frequency asymptote (PFA), and decreases in variability of functions fit to units sampled from preinflamed and noninflamed tissue (n = 23). Experiments were also conducted in which units were characterized before and after carrageenan treatment. In 7 of 10 cases, injection of carrageenan into the oral mucosal led to improved dynamic and/or static reactivity. Injection of vehicle led to changes in reactivity in one of five cases. 4. Carrageenan induced decreases in activation thresholds only when afferent receptive fields fell into restricted tissue zones. Large shifts in activation thresholds were observed for five of five (3 MNs and 2 IPRs) units in the sulcal zone of the incisal papilla (IP). In contrast, activation thresholds increased or remained the same in 11 of 12 units (10 IPRs and 3 MNs) with receptive fields in the medial or ventral tissue zones. Changes in activation threshold evolved slowly after carrageenan injection and required 1-2 h to develop. Rapid changes in activation threshold were also observed in a limited number of cases (3). These threshold shifts were unrelated to carrageenan inflammation. It was suggested that reliance on activation threshold as the sole method of assessing sensitization may produce false negatives. 5. It was suggested that shifts in PFTs slopes and mean response intervals of IPRs and MNs may contribute to the development of mechanical hyperalgesia.
AB - 1. We have previously described two classes of high-threshold mechanoreceptors (HTMs) of the oral mucosa of the goat. Mechanonociceptors (MNs) had very high thresholds (16-300 g) and were poor transducers of pressure. Intense pressure receptors (IPRs) had thresholds from 2 to 16 g and were good transducers of pressure. After carrageenan inflammation (CI) we observed mechanical sensitization in both classes of HTMs. The characteristics were as follows. 2. Sensitization of MNs was manifested as qualitative shifts in the capacity to encode intense pressure. MNs that were unable to code intensity before CI acquired pressure coding properties after treatment with carrageenan. Qualitative shifts in coding capacity were suggested by the greater proportion of MNs coding in preinflamed (10 of 14) compared with noninflamed tissue (8 of 25 cases). Improved afferent reactivity was directly observed, in additional experiments, in which MNs were characterized in normal tissue before the injection of carrageenan into the mucosa. In five of six cases, either qualitative or quantitative improvements were observed. In control experiments, improved reactivity was observed in one of six cases. 3. Sensitization in IPRs was manifested as both qualitative and quantitative improvement in intensity coding properties. Power functions fit to individual IPRs indicated sensitization for most mucosal afferents after inflammation. Carrageenan induced decreases in the mean response interval, pressure-frequency threshold (PFT), and pressure-frequency asymptote (PFA), and decreases in variability of functions fit to units sampled from preinflamed and noninflamed tissue (n = 23). Experiments were also conducted in which units were characterized before and after carrageenan treatment. In 7 of 10 cases, injection of carrageenan into the oral mucosal led to improved dynamic and/or static reactivity. Injection of vehicle led to changes in reactivity in one of five cases. 4. Carrageenan induced decreases in activation thresholds only when afferent receptive fields fell into restricted tissue zones. Large shifts in activation thresholds were observed for five of five (3 MNs and 2 IPRs) units in the sulcal zone of the incisal papilla (IP). In contrast, activation thresholds increased or remained the same in 11 of 12 units (10 IPRs and 3 MNs) with receptive fields in the medial or ventral tissue zones. Changes in activation threshold evolved slowly after carrageenan injection and required 1-2 h to develop. Rapid changes in activation threshold were also observed in a limited number of cases (3). These threshold shifts were unrelated to carrageenan inflammation. It was suggested that reliance on activation threshold as the sole method of assessing sensitization may produce false negatives. 5. It was suggested that shifts in PFTs slopes and mean response intervals of IPRs and MNs may contribute to the development of mechanical hyperalgesia.
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U2 - 10.1152/jn.1991.66.4.1280
DO - 10.1152/jn.1991.66.4.1280
M3 - Article
C2 - 1761984
AN - SCOPUS:0026095077
SN - 0022-3077
VL - 66
SP - 1280
EP - 1290
JO - Journal of neurophysiology
JF - Journal of neurophysiology
IS - 4
ER -