Hobbelen et al. determined the effect of the dose rate of a high-risk fungicide on the number of years that a high-risk fungicide can provide effective disease control in the selection phase for the same host-pathogen system. Their analyses showed that this number of years was constant or slightly decreased with increasing dose rate of the high-risk fungicide. Vincristine-treated rats displayed all of the behavioural characteristics of peripheral sensory neuropathy observed in this model, i.e. static and dynamic mechanical allodynia and hyperalgesia. As previously described in both patients and animal models, we observed that administration of oxycodone or morphine alleviated symptoms of chronic neuropathic pain. These observations are consistent with previous reports demonstrating morphine’s Delpazolid inefficacy in the symptomatic relief of neuropathic pain in STZ-induced diabetes models, as well as an observed slower rate of tolerance to oxycodone-6-oxyme as compared to morphine in naive animals. While morphine and oxycodone are both mopioid receptor agonists, previous studies have shown that these two opioids exhibit different efficiencies and distinct analgesic profiles in various pain models, such as the bone cancer pain model and the SNL model. A more recent study from that same group has shown that modification of the m-opioid receptor is responsible for the distinct analgesic effect of oxycodone and morphine, and that m-opioid receptor activation is less attenuated by oxycodone than by morphine. Although the authors of that study dismiss the hypothesis that, in the bone cancer pain model, a change in the number of m-opioid receptors or a change in the m-opioid receptor binding affinity might be the underlying mechanisms, these hypotheses remain valid in our model. Finally, as proposed by Nakamura et al., the differential activation of the mopioid receptor by oxycodone or morphine might be due to the mechanism that regulates GTP binding onto G proteins in the mreceptor. These changes in m-opioid receptor activation might produce subtle but functionally important variations in intracellular cascade signalling, possibly leading to a modified gene expression that is observed after oxycodone treatment, but not after morphine treatment. Previous studies have reported that repeated opiate administration alters gene expression in different regions of the nervous system in rodents, Angiotensin II human which may contribute to plastic changes associated with tolerance. It has also been shown that morphine treatment alters the expression of several receptors in the amygdala, including the GABAA receptor. Moreover, chronic treatment of morphine leads to a decrease in GABAergic tonus. Our DNA microarray analysis confirms this downregulation of GABAA receptor subunits in DRG neurons induced by chronic morphine treatment. The functional consequence of this decreased GABAA receptor synthesis in DRG neurons could be a reduction in the spinal pre-synaptic GABAergic tone, ultimately resulting in a persistent alteration of synaptic signalling. Our DNA microarray experiment was designed to address distinct yet complementary questions. First, which genes are differentially expressed by vincristine treatment at the end of the chronic analgesic treatment? This analysis is important to comprehending the mechanisms underlying the maintenance of neuropathic pain symptoms associated with vincristine treatment.