Ameboid receptive fields of cells in laminae 1, 2 and 3.
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Biomedical subjects
Publications and source records attributed to M Fitzgerald.
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1. Ninety-three polymodal nociceptor units with unmyelinated axons were isolated from rabbit sural nerves. Twenty-three were used for control data. These showed normal sensitization on repeated heating of their receptive fields, measured here as a drop in mean heat threshold. 2. Small injuries were made 5 (n = 15) or 10 (n = 12) mm outside the receptive fields of some polymodal nociceptors. This resulted in the development of spontaneous firing and lowered thresholds to heating of the receptive field. 3. Local anaesthetic previously injected into the site of injury blocked this spread of heat sensitization. Previous injection of saline had no effect. 4. Antidromic stimulation of the sural nerve, proximal to the recording site, also resulted in heat sensitization of polymodal nociceptors (n = 10). 5. Possible mechanisms for the spread of sensitization of polymodal nociceptors from nearby injury are discussed. Analogies are drawn between these results and those of Lewis (1935--36) on the spread of cutaneous ;yperalgesia around a skin injury in man.
Cellular reorganization in the pulp following mechanical pulp exposure involves three steps: First, lysis and macrophage resolution of the clot form; second, there is an invasion of the clot area by fibroblasts and endothelial cells, i.e., formation of granulation tissue; third, an organization and differentiation of these cells into functional odontoblasts occurs as early as 9 days after exposure. Autoradiographic results showed an increased DNA synthesis in the fibroblast and endothelial cell populations which coincided with a histologically-observed increase in those populations. A relative increase in fibroblastic activity, as compared to endothelial cell activity, suggested that fibroblasts may be the cells that replace odontoblasts.
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1. Seventy high threshold mechanoreceptor units (HTMs) with myelinated axons were isolated from the sural nerves of cats and rabbits. Thirteen cat and forty-two rabbit HTMs were testec by controlled, repeated heating of the skin of the foot or lower leg to noxious levels. 2. Many of the units (77% in the cat and 40% in the rabbit) fired to heating. Only six (11%) of these fired to the first brief heating to 50-55 degrees C. The rest required 2-6 heat trials before responding. 3. Heat responding units always became more sensitive with repeated heat stimulation but their mechanical sensitivity showed no comparable changes when heat sensitization occurred. 4. If these results are applicable to man, they suggest that HTMs play little role in generating the first pain that follows skin heating but that they may be involved in the increased sensitivity to heat pain (hyperalgesia) shown by skin previously injured by heating.
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