Abstract
Long-term potentiation (LTP) in nociceptive spinal pathways shares several features with hyperalgesia and has been proposed to be a cellular mechanism of pain amplification in acute and chronic pain states. Spinal LTP is typically induced by noxious input and has therefore been hypothesized to contribute to acute postoperative pain and to forms of chronic pain that develop from an initial painful event, peripheral inflammation or neuropathy. Under this assumption, preventing LTP induction may help to prevent the development of exaggerated postoperative pain and reversing established LTP may help to treat patients who have an LTP component to their chronic pain. Spinal LTP is also induced by abrupt opioid withdrawal, making it a possible mechanism of some forms of opioid-induced hyperalgesia. Here, we give an overview of targets for preventing LTP induction and modifying established LTP as identified in animal studies. We discuss which of the various symptoms of human experimental and clinical pain may be manifestations of spinal LTP, review the pharmacology of these possible human LTP manifestations and compare it to the pharmacology of spinal LTP in rodents.
Highlights
Pain arising from impending or actual tissue injury has an important physiological role, protecting the body from injury and promoting healing once injury has occurred
Section conclusions In conclusion, spinal long-term potentiation (LTP) induced by an initial injury or noxious input may contribute to both primary and secondary hyperalgesia
It must be emphasized that the above described sensory phenomena are compatible with spinal LTP, they may be explained by other mechanisms
Summary
Pain arising from impending or actual tissue injury has an important physiological role, protecting the body from injury and promoting healing once injury has occurred. There are currently two methods to record synaptic strength in nociceptive pathways that fulfil the above requirements [2,27] Both investigate the synaptic connection between primary afferent C-fibres (many of which are nociceptive) and superficial dorsal horn neurons, which is the focus of the present review. Synaptic strength between primary afferent Cfibres and superficial dorsal horn neurons can be measured in adult rodents by stimulating the sciatic nerve and recording C-fibre-evoked field potentials in superficial dorsal horn that are known to reflect summation of postsynaptic, mainly monosynaptically evoked currents [3,28]. Induction of LTP in rodent spinal nociceptive pathways LTP at the synapse between primary afferent C-fibres and superficial dorsal horn neurons can be induced by various protocols, including strong noxious stimulation of the input pathway and application of certain drugs (Table 1).
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