Pain
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A midline dorsal column lesion has been shown to be an effective surgical treatment for the relief of pelvic visceral pain in patients. The aim of this study was to examine the effectiveness of a dorsal column lesion upon: (i) increased electrophysiological responses of neurons in the ventral posterolateral thalamic nucleus in anesthetized rats evoked by the application of bradykinin to the surface of the pancreas, and (ii) pain-related behaviors observed after pancreatic infusion with bradykinin. In rats anesthetized with pentobarbital, recordings from individual thalamic neurons were made using tungsten electrodes. ⋯ A dorsal column lesion made prior (1 week) to the bradykinin infusion reduced the decrease in exploratory behavior but did not return exploratory behavior to control levels. In conclusion, nociceptive information relayed to the thalamus about the pancreas is transmitted from the spinal cord through the dorsal columns, possibly by the post-synaptic dorsal column pathway. However, the dorsal column pathway may not be the sole route for relaying information about noxious stimulation of the pancreas, particularly that impacting complex behavioral responses.
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Recent studies suggest that opioids can produce analgesia through peripheral mechanisms following inflammation of peripheral tissue. This study examined whether opioids administered prior to inflammation can produce antinociception by peripheral mechanisms in a model of visceral pain. Mice were injected intraperitoneally (i.p.) with 1% acetic acid to evoke abdominal writhing, a standard model of visceral pain. ⋯ The highest dose (10 microg) was ineffective when given intravenously 5 min before acetic acid, suggesting that antinociception following i.p. administration was acting via peripheral mechanisms. These data demonstrate that low doses of opioids, given before or after acetic acid, produce visceral antinociception through peripheral mechanisms. This may be clinically relevant for the management of postoperative abdominal pain.
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Anatomical studies demonstrate the presence of glutamate receptors on unmyelinated axons in peripheral cutaneous nerves. Pharmacological studies show that intraplantar injection of glutamate or glutamate agonists in the glabrous skin results in nociceptive behaviors. The present study describes a novel in vitro skin-nerve preparation using the glabrous skin from the rat hindpaw. ⋯ Exposure of A delta or C fibers to glutamate did not result in a decrease in von Frey thresholds. These data provide a physiological basis for the nociceptive behaviors that arise following intraplantar injection of glutamate or glutamate agonists. Furthermore, demonstration of glutamate-induced excitation and heat sensitization of nociceptors indicates that local or topical administration of glutamate receptor antagonists may have therapeutic potential for the treatment of pain.
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Nerve growth factor (NGF) regulates the nociceptive properties including sensitivity to capsaicin of a subset of dorsal root ganglion neurons, which express the high-affinity NGF receptor, trkA. Capsaicin sensitivity co-localizes with the expression of a cloned capsaicin receptor, vanilloid receptor type 1 (VR-1), which displays properties similar to the native capsaicin response. ⋯ NGF treatment increased both VR-1 mRNA expression and capsaicin evoked release of CGRP. These effects were inhibited by treatment with the trkA inhibitor k252a.