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  4. Role of GPCR (mu-opioid)-receptor tyrosine kinase (epidermal growth factor) crosstalk in opioid-induced hyperalgesic priming (type II).

Role of GPCR (mu-opioid)-receptor tyrosine kinase (epidermal growth factor) crosstalk in opioid-induced hyperalgesic priming (type II).

Araldi D, Ferrari LF, Levine JD (2018) Role of GPCR (mu-opioid)-receptor tyrosine kinase (epidermal growth factor) crosstalk in opioid-induced hyperalgesic priming (type II). Pain 159(5):864-875. doi: 10.1097/j.pain.0000000000001155

Objective: To determine the the mechanisms mediating the induction of opioid-induced hyperalgesia and the prolongation of prostaglandinE2-induced hyperalgesia in type II hyperalgesic priming.

Summary: Understanding the mechanisms responsible for the induction of type II hyperalgesic priming, a form of neuroplasticity in the peripheral terminal of the primary afferent nociceptor, may provide useful information for the design of drugs with improved therapeutic profiles to treat neuroplasticity induced by chronic use of opioids.

Usage: SSP-SAP was prepared in saline (5 ng/mL), and 20 mL was injected intrathecally into rats, 14 days before nociceptive tests.

Related Products: SSP-SAP (Cat. #IT-11)