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We have evaluated the pattern of c-fos expression induced in the rat spinal cord, caudal brainstem and cerebellum by a behavior that is associated with non-noxious inputs transmitted over large-diameter primary afferent fibers, namely walking for 1 h on a rotating rod. Walking on the rotating rod induced a large increase in the number of Fos-like(More)
1. This study examined sensory neurons in the saphenous nerve of rats treated with streptozotocin to induce diabetes (STZ-D). Several physiological properties of sensory neurons were not significantly different in STZ-D compared with control (CON) rats, including percentage and rate of spontaneous activity seen in the whole nerve and mechanical and thermal(More)
1. We have previously demonstrated that although rats with streptozotocin-induced diabetes (STZ-D) have decreased behavioral mechanical nociceptive thresholds (hyperalgesia), their C-fiber primary afferent mechanical (von Frey hair) thresholds are not altered. Instead, when stimulated with a standardized sustained suprathreshold mechanical stimulus,(More)
To compare changes in primary afferent nociceptors associated with inflammatory versus neuropathic hyperalgesia, we evaluated in rats the mechanical stimulus-response function of isolated C-fiber primary afferent nociceptors to 10-s stimuli of differing mechanical strengths; 36 fibers after prostaglandin E2, 28 fibers from streptozotocin-diabetic rats and(More)
C-Fiber mechanoheat (C-MH) nociceptors from the saphenous nerve were studied, in control rats and in rats that underwent surgical sympathectomy. Intradermal injection, alone, of either norepinephrine (NE) or the calcium ionophore, A23187, did not affect mechanical threshold. The combination of A23187 and NE, however, significantly decreased mechanical(More)
Behavioral studies have shown that mechanical hyperalgesia induced by intradermal injection of prostaglandin E2 is blocked by inhibitors of the cAMP second messenger system. Similarly, injection of prostaglandin E2 also induces a decrease in mechanical threshold and an increase in the number of action potentials elicited by test stimuli in most C-fibre(More)
It has been suggested that the mechanism underlying the pain that occurs in patients with diabetic neuropathy may be similar to that mediating sympathetically maintained pain (SMP), such as occurs in patients with reflex sympathetic dystrophy. To evaluate this suggestion we have examined a model of diabetes mellitus, the streptozotocin-diabetic (STZ-D) rat,(More)
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