2011
DOI: 10.1016/j.sjpain.2011.06.003
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Neuropathic pain models in the development of analgesic drugs

Abstract: Introduction Animal disease models are predictive for signs seen in disease. They may rarely mimic all signs in a specific disease in humans with respect to etiology, cause or development. Several models have been developed for different pain states and the alteration of behavior has been interpreted as a response to external stimulus or expression of pain or discomfort. Considerable attention must be paid not to interpret other effects such as somnolence or motor impairment as a pain response and similarly no… Show more

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Cited by 17 publications
(8 citation statements)
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“…Neuropathy complications result from toxic effects of chronic hyperglycemia combined with other metabolic derangements that afflict diabetic patients (Moore et al, 2009). Pharmacologic treatment currently used in the management of neuropathic pain include: sodium channels blockers attenuating the pain signal, calcium channel blockers diminishing calcium influx into pain signaling cells mediated through the a2d-subunit site, opioids strengthening the response of enkephalins/ endorphins to inhibit pain signaling in the spinal dorsal horn, neurotransmitter modulators enhancing serotonin and/or noradrenaline/acetylcholine/GABA availability in the pain inhibitory descending pathways, and interference in the prostaglandin cascade (Honore et al, 2011). These above treatment also require daily regimens that may require slow titration or involve inconvenient multiple daily doses, which, in turn, could potentially impact compliance (Tolle, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…Neuropathy complications result from toxic effects of chronic hyperglycemia combined with other metabolic derangements that afflict diabetic patients (Moore et al, 2009). Pharmacologic treatment currently used in the management of neuropathic pain include: sodium channels blockers attenuating the pain signal, calcium channel blockers diminishing calcium influx into pain signaling cells mediated through the a2d-subunit site, opioids strengthening the response of enkephalins/ endorphins to inhibit pain signaling in the spinal dorsal horn, neurotransmitter modulators enhancing serotonin and/or noradrenaline/acetylcholine/GABA availability in the pain inhibitory descending pathways, and interference in the prostaglandin cascade (Honore et al, 2011). These above treatment also require daily regimens that may require slow titration or involve inconvenient multiple daily doses, which, in turn, could potentially impact compliance (Tolle, 2010).…”
Section: Introductionmentioning
confidence: 99%
“…by spinal nerve ligation [14]. The unilateral ligation of two spinal nerves (L 5 and L 6 ) was performed under pentobarbitone anaesthesia (50 mg/kg i.p.)…”
Section: Methodsmentioning
confidence: 99%
“…When comparing various experimental models of neuropathy (Honoré et al 2011), among advantages of the model induced by unilateral ligation of spinal nerves L5 and L6 is that it provides a possibility to use the easily accessible plantar skin as test site and, therefore, the SNL model of neuropathy described in detail elsewhere (Kim and Chung 1992) was used in the present study. Briefly, after induction of a deep level of anesthesia as described above, separation of left paraspinal muscles from spinous processes provided access to the spinal segment L6.…”
Section: Induction Of Experimental Neuropathy and Determination Of Mementioning
confidence: 99%