(NA) is a key neurotransmitter of the endogenous pain inhibitory system.
Peripheral nociceptive stimuli activate noradrenergic brainstem projections
to the spinal cord, resulting in antinociception and inhibition of spinal
nociceptive neurons. Lesion or inhibition of noradrenergic spinal afferents,
in contrast, produces a state of acute hyperalgesia and reduced antinociceptive
effects of opiates.
The DBH -/- mice also allow us to verify a number of hypotheses on the mechanism of pain in fibromyalgia. Fibromyalgia is common pain disorder that affects approximately 2% of the general population. Fibromyalgia patients have a decreased threshold for pain and decreased response to opiates. There has been a considerable effort through clinical research to find the etiology of this disease, which resulted in the identification of decreased levels of noradrenaline's principal metabolite (3-methoxy-4-hydroxyphenethylene) in fibromyalgia patients.
Research in animal models of decreased endogenous pain inhibition now allow us to test the hypothesis that the pain encountered in fibromyalgia patients is related to the observed decrease in noradrenaline. While we believe that other variables could be involved in the pathogenesis of fibromyalgia, the proposed mouse model will allow us to isolate one variable, the noradrenergic system, and test the impact of its dysfunction on complex pain behaviors and opiate analgesia.
Site prepared and maintained by : Gabriella Janni