These data demonstrate the efficacy of the preproenkephalin A encoding vector and suggest that it should help in elucidating the role of Met-enkephalin-containing primary afferent fibers in pain transmission and/or control.
We previously reported that polymer-encapsulated mouse neuroblastoma cells that are capable of secreting beta-endorphin may reduce pain sensitivity in rats after capsule implantation into the cerebrospinal fluid (CSF)-filled subarachnoid space of the spinal cord.
Transplantation of beta-endorphin-secreting cells into brain or spinal cord may provide a gene therapy approach for the treatment of chronic, opioid-sensitive pain states.
Immune cell-derived beta-endorphin (END) and other opioid peptides elicit potent and clinically relevant inhibition of pain (analgesia) in inflamed tissue by activation of peripheral opioid receptors.
In this study, we report that α-MSH suppresses the transient outward A-type K<sup>+</sup> current (<i>I</i><sub>A</sub>) in trigeminal ganglion (TG) neurons and thereby modulates neuronal excitability and peripheral pain sensitivity in rats.
Physiological parameters (heart rate, respiratory rate, rectal temperature, invasive blood pressure, cortisol, β-endorphin, interleukin-1β, interleukin-6, tumor necrosis factor-α and haptoglobin plasmatic concentration), local variables (tactile sensitivity score, pressure pain thresholds and horn temperature), behavior and pain scores [multidimensional pain scale and visual analogue scale (VAS)] were assessed at baseline and at several pre-determined time points until 24h after disbudding.
The aim of this work is to evaluate the effects of transcranial direct current stimulation (tDCS) in relieving fibromyalgia pain and its relation with beta-endorphin changes.
We review recent findings on molecular adaptations in sustained pain models, and propose how these adaptations (including sustained release of the endogenous mu-agonist beta-endorphin) can result in decreased abuse potential of mu-agonists in chronic pain states.
The enhanced expression of endogenous opioid peptides, including β-endorphin, has been implicated in the mechanism of action of pulsed radio frequency (PRF) application in pain modulation.
This study investigated the effects of intracerebroventricular (ICV) and intra-arcuate nucleus (ARC) injection of ghrelin on pain behavioral responses and levels of β-endorphin (β-EP) and met-enkephalin (MENK) in the periaqueductal gray area (PAG) during the formalin test in rats.
Intrathecal administrations of the POMC vector elevated spinal beta-endorphin levels, as manifested in a significantly elevated pain threshold for the CCI limbs.
Regression analyses indicated that β-endorphin level was negatively related to pressure pain threshold (β = -17.18, <i>p</i> = .02) and positively related to punctate mechanical pain (β = 17.13, <i>p</i> = .04), after controlling for age, gender, and OA severity.