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The nociceptive flexion reflex paradigm is widely used to investigate modulation of nociception and represents a reliable objective measure of the functional activation of the nociceptive network.
Previous studies indicate that descending modulation of nociception is progressively increased following persistent inflammation.
Bajic, D. & Proudfit, H.K. Projections of neurons in the periaqueductal gray to pontine and medullary catecholamine cell groups involved in the modulation of nociception.
Despite the importance of the periaqueductal gray (PAG) in the modulation of nociception and pain, many aspects of the roles of the different columns of the PAG in descending controls: facilitation and inhibition, are not understood.
In a previous study, we showed in rats that axons of some locus coeruleus/subcoeruleus (LC/SC) neurons involved in coeruleospinal modulation of nociception descend through the ipsilateral side of the spinal cord and cross the midline at spinal segmental levels.
The first investigations on the modulation of nociception by vagal afferents were performed approximately 20 years ago [83 85].
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In human studies, NFR responsiveness has been used as a direct measure of nociception as well as an indirect measure of supraspinal modulation of nociceptive transmission.
Modulation of spinal nociception from the anterior hypothalamus/preoptic area (AH/POA), and consequent alterations in the pain experience may contribute to integrated responses brought into play during fear or stress and as part of the sickness response.
Several studies have demonstrated that P2X7 is involved in the modulation of pathological nociception.
This study demonstrates a robust effect of benzodiazepine receptor modulation of the nociception specific blink reflex (nBR) without any μ-opiate or glutamate NMDA receptor component.
These data provide direct evidence that a peripheral cannabinoid mechanism suppresses the development of inflammation-evoked neuronal activity at the level of the spinal dorsal horn and implicate a role for CB(2) and CB(1) in peripheral cannabinoid modulation of inflammatory nociception.
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