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- W2021738503 abstract "Exposure to opioids can induce a state of latent sensitization characterized by long-lasting enhanced responses to subsequent cutaneous injury. Here, we explored the possibility that prior treatment with morphine could induce a state of latent sensitization to visceral pain conditions. Following butyrate enemas to induce non-inflammatory visceral pain, acute morphine administration produced dose-related inhibition of referred viscerosomatic hypersensitivity. Treatment with morphine for a period of six days resulted in a persistent hyperalgesia that resolved many days after termination of drug administration. In morphine pre-exposed rats, butyrate-induced referred hypersensitivity was enhanced and extended in duration. No differences were observed in the morphine dose-response curve in suppression of acute nociception (i.e., the hot-plate assay) when morphine pre-exposed rats were compared to naïve rats indicating that opioid antinociceptive tolerance was not present. However, the morphine dose-response curve to suppress evoked viscerosomatic hypersensitivity was displaced to the right by approximately 4-fold in morphine pre-exposed rats. Induction of viscerosomatic hypersensitivity resulted in an increased labeling of CGRP-, but not substance P-positive cells in the lumbar dorsal root ganglia; increased labeling was not affected by prior exposure to morphine. The data indicate that a period of morphine exposure can induce a state of latent sensitization to subsequent visceral pain characterized by extended duration of hypersensitivity. This condition likely reflects enhanced visceral pain intensity as a consequence of persistent pronociceptive adaptive changes." @default.
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- W2021738503 date "2010-10-01" @default.
- W2021738503 modified "2023-10-18" @default.
- W2021738503 title "Opioid-induced latent sensitization in a model of non-inflammatory viscerosomatic hypersensitivity" @default.
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- W2021738503 doi "https://doi.org/10.1016/j.brainres.2010.08.032" @default.
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