Hindawi Publishing Corporation Pain Research and Treatment Volume 2012, Article ID 143579, 5 pages doi:10.1155/2012/143579 Research Article Evaluation of Lercanidipine in Paclitaxel-Induced Neuropathic Pain Model in Rat: A Preliminary Study Lekha Saha, Debasish Hota, and Amitava Chakrabarti Department of Pharmacology, PGIMER, Chandigarh 160012, India Correspondence should be addressed to Lekha Saha, lekhasaha@rediffmail.com Received 9 July 2011; Revised 29 October 2011; Accepted 20 November 2011 Academic Editor: Donald A. Simone Copyright © 2012 Lekha Saha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. To demonstrate the antinociceptive effect of lercanidipine in paclitaxel-induced neuropathy model in rat. Materials and Methods. A total of 30 rats were divided into five groups of six rats in each group as follows: Gr I: 0.9% NaCl, Gr II: paclitaxel + 0.9% NaCl, Gr III: paclitaxel + lercanidipine 0.5 μg/kg, Gr IV: paclitaxel + lercanidipine 1 μg/kg, and Gr V: paclitaxel + lercanidipine 2.5 μg/kg. Paclitaxel-induced neuropathic pain in rat was produced by single intraperitoneal (i.p.) injection of 1 mg/kg of paclitaxel on four alternate days (0, 2, 4, and 6). The tail flick and cold allodynia methods were used for assessing the pain threshold, and the assessments were done on days 0 (before first dose of paclitaxel) and on days 7, 14, 21, and 28. Results. There was a significant decrease (P< 0.001) in the tail flick and cold allodynia latency in the paclitaxel-alone group from day 14 onward when compared with day 0. In the lercanidipine groups, the decrease in the tail flick and cold allodynia latency was not observed in 1.0 and 2.5 μg/kg groups and it was statistically significant (P< 0.01) when compared with paclitaxel-alone group. 1. Introduction Neuropathic pain is a type of pain which is caused by damage to or dysfunction of the nervous system. [1] Neuropathic pain cannot be explained by a single disease process or a single specific location of damage. It is a disorder in the structure and function of peripheral, motor, sensory, and/or autonomic neurons either partially or completely [2]. Neuro- pathic pain may be divided into peripheral, central, or mixed (peripheral and central) neuropathic pain. As much as 7% to 8% of the population is affected and in 5%, it may be severe [3]. In order to evaluate the mechanisms of neuropathic pain and to find new therapeutic approaches, different experimental neuropathic pain models have been developed which include chronic constriction injury of sciatic nerve, partial sciatic nerve ligation, and partial transaction of sciatic nerve. Current knowledge regarding the mechanisms of neuropathic pain is incomplete and is biased by a focus on animal models of peripheral nerve injury, and the treatment is often unsatis- factory. It is an area of largely unmet therapeutic need. The current pharmacological mainstays of clinical management are tricyclic antidepressants and certain anticonvulsants, but these only achieve clinically significant (>50%) pain relief in 40–60% of patients and are associated with several side effects. Opioids are generally considered to be less effective in neuropathic pain than in inflammatory pain [4]. Paclitaxel, a commonly used antineoplastic drug can pro- duce a dose-limiting painful peripheral neuropathy when given intraperitoneally and can be used as a model of peripheral neu- ropathy to evaluate the effect of various drugs in neuropathic pain [5]. Lercanidipine is a third-generation L-type calcium chan- nel blocker (CCB) belonging to the class dihydropyridines and is approved for the treatment of cardiovascular disor- ders. Various preclinical studies point to an altered role of voltage-gated Ca 2+ channels, particularly the α-2 delta sub- unit after neuropathy, and specific blockers have been shown to differentially attenuate the behavioural hypersensitivities and altered dorsal horn neuronal responses that accompany experimental neuropathic pain. The studies done to evaluate the action of CCBs on CNS are quite limited [6]. In the published literatures, there is no data available regarding the modulation of paclitaxel-induced neuropathic