Tags

Type your tag names separated by a space and hit enter

Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain.
Brain Res. 2004 Aug 27; 1018(2):159-70.BR

Abstract

Recently, our laboratory has proposed the avulsion of rat brachial plexus as a new and reliable model for the study of neuropathic pain. In this model, the neuropathy can be detected even at distant sites from the injury, both in ipsilateral and contralateral hindpaws. The purpose of this study was to pharmacologically characterise this behavioural model of persistent peripheral neuropathic pain by assessing the effects of several analgesic drugs currently used in clinical practice. For this purpose, the effects of these drugs on the mechanical and cold allodynia were analysed 20-40 days after rat brachial plexus avulsion. Injection of saline, administered by the same route as the other drugs, did not significantly affect the nociceptive threshold either in sham-operated or in neuropathic rats. However, administration of the opioid analgesic morphine (5 mg/kg, s.c.), the alpha2 adrenoceptor agonist clonidine (300 microg/kg, i.p.), the NMDA receptor antagonist ketamine (25 mg/kg, i.p.) or the anticonvulsant drug gabapentin (70 mg/kg, p.o.) consistently reduced both mechanical and cold allodynia following avulsion of rat brachial plexus. The administration of the selective COX-2 inhibitor celecoxib (10 mg/kg, p.o.) blocked mechanical allodynia, but not cold allodynia, whereas the sodium channel blocker lidocaine (40 mg/kg, i.p.) attenuated only cold allodynia. The non-steroidal anti-inflammatory drug diclofenac (100 mg/kg, i.p.), the steroidal anti-inflammatory dexamethasone (1.5 mg/kg, i.p.) and the antidepressant imipramine (10 mg/kg, i.p.) all failed to significantly attenuate both mechanical and cold allodynia in the rats following avulsion of brachial plexus. These findings suggest that avulsion-associated mechanical and cold allodynia, two classic signs of persistent neuropathic pain, were consistently prevented by several analgesics currently available in clinical practice, namely morphine, clonidine, ketamine and gabapentin, and to a lesser extent by celecoxib and lidocaine. Therefore, this new proposed model of persistent nociception seems to be suitable for the study of the underlying mechanisms involved in neuropathic pain and for the identification of potential clinically relevant drugs to treat this aspect of peripheral neuropathy.

Authors+Show Affiliations

Department of Pharmacology, Centre of Biological Sciences, Universidade Federal de Santa Catarina, Rua Ferreira Lima 82, Florianópolis, SC 88015-420, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15276874

Citation

Rodrigues-Filho, Rubens, et al. "Pharmacological Characterisation of the Rat Brachial Plexus Avulsion Model of Neuropathic Pain." Brain Research, vol. 1018, no. 2, 2004, pp. 159-70.
Rodrigues-Filho R, Campos MM, Ferreira J, et al. Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain. Brain Res. 2004;1018(2):159-70.
Rodrigues-Filho, R., Campos, M. M., Ferreira, J., Santos, A. R., Bertelli, J. A., & Calixto, J. B. (2004). Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain. Brain Research, 1018(2), 159-70.
Rodrigues-Filho R, et al. Pharmacological Characterisation of the Rat Brachial Plexus Avulsion Model of Neuropathic Pain. Brain Res. 2004 Aug 27;1018(2):159-70. PubMed PMID: 15276874.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pharmacological characterisation of the rat brachial plexus avulsion model of neuropathic pain. AU - Rodrigues-Filho,Rubens, AU - Campos,Maria Martha, AU - Ferreira,Juliano, AU - Santos,Adair R S, AU - Bertelli,Jayme A, AU - Calixto,João B, PY - 2004/05/25/accepted PY - 2004/7/28/pubmed PY - 2004/10/30/medline PY - 2004/7/28/entrez SP - 159 EP - 70 JF - Brain research JO - Brain Res VL - 1018 IS - 2 N2 - Recently, our laboratory has proposed the avulsion of rat brachial plexus as a new and reliable model for the study of neuropathic pain. In this model, the neuropathy can be detected even at distant sites from the injury, both in ipsilateral and contralateral hindpaws. The purpose of this study was to pharmacologically characterise this behavioural model of persistent peripheral neuropathic pain by assessing the effects of several analgesic drugs currently used in clinical practice. For this purpose, the effects of these drugs on the mechanical and cold allodynia were analysed 20-40 days after rat brachial plexus avulsion. Injection of saline, administered by the same route as the other drugs, did not significantly affect the nociceptive threshold either in sham-operated or in neuropathic rats. However, administration of the opioid analgesic morphine (5 mg/kg, s.c.), the alpha2 adrenoceptor agonist clonidine (300 microg/kg, i.p.), the NMDA receptor antagonist ketamine (25 mg/kg, i.p.) or the anticonvulsant drug gabapentin (70 mg/kg, p.o.) consistently reduced both mechanical and cold allodynia following avulsion of rat brachial plexus. The administration of the selective COX-2 inhibitor celecoxib (10 mg/kg, p.o.) blocked mechanical allodynia, but not cold allodynia, whereas the sodium channel blocker lidocaine (40 mg/kg, i.p.) attenuated only cold allodynia. The non-steroidal anti-inflammatory drug diclofenac (100 mg/kg, i.p.), the steroidal anti-inflammatory dexamethasone (1.5 mg/kg, i.p.) and the antidepressant imipramine (10 mg/kg, i.p.) all failed to significantly attenuate both mechanical and cold allodynia in the rats following avulsion of brachial plexus. These findings suggest that avulsion-associated mechanical and cold allodynia, two classic signs of persistent neuropathic pain, were consistently prevented by several analgesics currently available in clinical practice, namely morphine, clonidine, ketamine and gabapentin, and to a lesser extent by celecoxib and lidocaine. Therefore, this new proposed model of persistent nociception seems to be suitable for the study of the underlying mechanisms involved in neuropathic pain and for the identification of potential clinically relevant drugs to treat this aspect of peripheral neuropathy. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/15276874/Pharmacological_characterisation_of_the_rat_brachial_plexus_avulsion_model_of_neuropathic_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006899304008388 DB - PRIME DP - Unbound Medicine ER -