The mAb-based passive immunization studies reported earlier failed to confer complete infection sterilization and protection against different challenge routes. Prior to in vivo challenge studies, and also elucidation of the mode of protection they confer to the host is considerable in selection of promising monoclonal antibody to fight against B. pseudomallei infections. Approximately 7–8% of the European population suffers from neuropathic pain, and 5% of these cases may be severe. Unfortunately, the pharmacotherapy of neuropathic pain is frequently unsatisfactory for patients. One reason for their poor efficacy is CA-074 the lack of a clear understanding of the neurobiological mechanisms that underlie neuropathic pain. Morphine is the most commonly used opioid analgesic in the past 30 years. However, repeated use of opioids induces a tolerance phenomenon, which significantly reduces their analgesic effects. Among clinically used opioids, oxycodone shows excellent anti-hyperalgesic and antiallodynic effects against neuropathic pain. Oxycodone is a semi-synthetic opioid analgesic, and has been used in clinics since 1917. Like other opioids, including morphine, the analgesic effect of oxycodone is mainly mediated through the activation of the m-opioid receptor. Interestingly, the analgesic effect of oxycodone seems to be as potent as morphine on different types of pain, including visceral pain, post-operative pain and cancer pain. Moreover, the oxycodone-paracetamol combination was shown to be effective against chronic lower back pain, whereas morphine treatment did not show any beneficial effect. In patients with neuropathic pain, oxycodone treatment improves health-related quality of life and diminishes the impact of pain on physical activity and sleep. However, the neurobiological mechanisms underlying the therapeutic action of these two opioids are currently only partially understood. The aim of this study was to identify the molecular changes that produce the different analgesic effects of morphine and oxycodone. Vincristine is an anti-neoplasic drug used to treat a wide variety of cancers. Nonetheless,KPT330 Selinexor it induces a peripheral neurotoxicity and subsequent neuropathic pain in both patients and animal models. Here, we observed in an animal model of vincristine-induced neuropathic pain that oxycodone has a longer lasting analgesic effect than morphine. Based on DNA microarray technology in dorsal root ganglia, we report an important list of genes that are differentially expressed in oxycodone-treated rats, as compared to morphine-treated subjects. This provides clues on the mechanisms underlying their different long-term actions. Furthermore, we provide direct evidence for an involvement of GABAB receptors in the long-lasting effect of oxycodone on neuropathic pain. The aim of this study was two-fold: to better understand the mechanisms underlying the analgesic effect of both oxycodone and morphine; and to compare these mechanisms of action in a model of neuropathic pain induced by vincristine. Our results demonstrate that a large number of genes are dysregulated after opioid analgesic treatment in vincristine-treated animals. These findings also suggest an increased GABAergic tone in the superficial dorsal horn induced by oxycodone treatment that is mediated by GABAB2 receptor; this would explain the enhanced alleviation of chronic neuropathic pain that we observed.