Characterization of μ Opioid Receptor Binding and G Protein Coupling in Rat Hypothalamus, Spinal Cord, and Primary Afferent Neurons during Inflammatory Pain

Abstract

ABSTRACT

Persistent pain model reveals sex difference in morphine potency

“…Several mechanisms have been proposed to account for persistent inflammation-induced changes in opioid potency, including upregulation of glutamate receptors in the RVM (24,25), increased MOR expression and second messenger coupling in the lumbar dorsal root ganglia (51,60), and increased release of endogenous opioids in several supraspinal sites, including the PAG and RVM (27,53,59). These results together suggest that in males, multiple mechanisms contribute to persistent pain-induced changes in opioid potency.…”

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

“…In addition, G protein coupling of opioid receptors was augmented (Zöllner et al, 2003;Shaqura et al, 2004). Extracellular recordings from peripheral sensory nerve fibers demonstrated opioid inhibition of spontaneous and stimulus-evoked action potentials in models of tissue injury Andreev et al, 1994;Junger et al, 2002;Wenk et al, 2006).…”

Role of peripheral μ‐opioid receptors in arthritis: Are they potential targets for therapy?

“…Increased axonal transport is preceded by up-regulation of messenger RNA (mRNA) transcription in response to inflammation, which is dependent on neuronal electrical activity (21). The increased number of -opioid receptors on peripheral afferent fibers could contribute to enhanced analgesic effects of endogenous, mainly leukocyte-derived, opioid peptides and also exogenously administered ligands such as morphine (13,(20)(21)(22). There is evidence of the presence of functionally active -opioid receptors in rat, canine, and human articular chondrocytes isolated from osteoarthritic knees at both the mRNA and protein levels (23).…”

“…First, the experimental rat model they used is a monarthritis model in which the adjuvant is injected directly into the articular space to induce an isolated destructive inflammation of the respective knee joint without soft tissue involvement. In contrast, other investigators administered CFA intraplantarly for the induction of unilateral hind paw inflammation (20)(21)(22) or intradermally into the root of the tail to evoke polyarthritis (13).…”

“…In other models of inflammation in which up-regulation of -opioid receptors in the peripheral tissues and in the ipsilateral dorsal root ganglia in response to an intraplantar injection of the adjuvant was investigated, the maximum observation period was 96 hours (19)(20)(21)(22)(23). At that time, simultaneously increased axonal transport (20) and enhanced transcription were observed (21).…”