Systemic fentanyl induces hyperalgesic priming, long-lasting neuroplasticity in nociceptor
function characterized by prolongation of inflammatory mediator hyperalgesia. To evaluate …

Clinical µ-opioid receptor (MOR) agonists produce hyperalgesic priming, a form of
maladaptive nociceptor neuroplasticity, resulting in pain chronification. We have established …

Hyperalgesic priming, a form of neuroplasticity in nociceptors, is a model of the transition
from acute to chronic pain in the rat, which involves signaling from the site of an acute tissue …

We investigated the dose dependence of the role of nociceptors in opioid-induced side-
effects, hyperalgesia and pain chronification, in the rat. Systemic morphine produced a dose …

Opioid-induced hyperalgesia (OIH) is a serious adverse event produced by opioid
analgesics. Lack of an in vitro model has hindered study of its underlying mechanisms …

We have previously developed a model in the rat for the transition from acute to chronic
pain, hyperalgesic priming, in which a long-lasting neuroplastic change in signaling …

The primary afferent nociceptor was used as a model system to study mechanisms of pain
induced by chronic opioid administration. Repeated intradermal injection of the selective mu …

We previously developed a model of opioid-induced neuroplasticity in the peripheral
terminal of the nociceptor that could contribute to opioid-induced hyperalgesia, type II …

Acute insults produce hyperalgesic priming, a neuroplastic change in nociceptors that
markedly prolongs inflammatory mediator-induced hyperalgesia. After an acute initiating …

Stimulation of the mu-opioid receptor (MOR) on nociceptors with fentanyl can produce
hyperalgesia (opioid-induced hyperalgesia, OIH) and hyperalgesic priming, a model of …