ArticleYonsei medical journal2007
Antiallodynic effect of pregabalin in rat models of sympathetically maintained and sympathetic independent neuropathic pain.
Article in Yonsei medical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Spinal TRPA1 Contributes to the Mechanical Hypersensitivity Effect Induced by Netrin-1.International journal of molecular sciences · 2022Article
- Article
- Response to pregabalin and progesterone differs in male and female rat models of neuropathic and cancer pain.Canadian journal of pain = Revue canadienne de la douleur · 2020Article
- Neuropathic pain modulation after spinal cord injury by breathing-controlled electrical stimulation (BreEStim) is associated with restoration of autonomic dysfunction.Journal of pain research · 2018Article
- Effect of Pregabalin on Cardiovascular Responses to Exercise and Postexercise Pain and Fatigue in Fibromyalgia: A Randomized, Double-Blind, Crossover Pilot Study.Pain research and treatment · 2015Article
- Alpha 2 Delta (α(2)δ) Ligands, Gabapentin and Pregabalin: What is the Evidence for Potential Use of These Ligands in Irritable Bowel Syndrome.Frontiers in pharmacology · 2011Article
- Evidence that pregabalin reduces neuropathic pain by inhibiting the spinal release of glutamate.Journal of neurochemistry · 2010Article
- Article
- The antiallodynic action of pregabalin may depend on the suppression of spinal neuronal hyperexcitability in rats with spared nerve injury.Pain research & managementArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pregabalin binds to the voltage-dependent calcium channel alpha2delta subunit and modulates the release of neurotransmitters, resulting in analgesic effects on neuropathic pain. Neuropathic pain has both sympathetically maintained pain (SMP) and sympathetic independent pain (SIP) components. We studied the antiallodynic effects of pregabalin on tactile allodynia (TA) and cold allodynia (CA) in SMP-and SIP-dominant neuropathic pain models. Allodynia was induced by ligation of the L5 and L6 spinal nerves (SMP model) or by transection of the tibial and sural nerves (SIP model) in rats. For intrathecal drug administration, a PE-10 catheter was implanted through the atlantooccipital membrane to the lumbar enlargement. Pregabalin was administered either intraperitoneally (IP) or intrathecally (IT) and dosed up incrementally until an antiallodynic effect without sedation or motor impairment was apparent. TA was assessed using von Frey filaments, and CA was assessed using acetone drops. IP-administered pregabalin dose-dependently attenuated TA in both models and CA in the SMP model, but not CA in the SIP model. IT-administered pregabalin dose-dependently attenuated both TA and CA in both models. However, the dose response curve of IT-administered pregabalin in SMP was shifted to left from that of SIP and the ED50 of IT-administered pregabalin for CA in SMP was about 900 times less than that in SIP. These findings suggest that pregabalin exerts its antiallodynic effect mainly by acting at the spinal cord, and that IT-administered pregabalin has more potent antiallodynic effects in SMP. The alpha2delta subunit might be less involved in the CA in SIP.
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