Ketamine Induced Analgesia in Mice at Sub-psychotomimetic Dose
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Date
2017-01
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West African Journal of Pharmacology and Drug Research
Abstract
The roles of N- Methyl –D- Aspartate receptor in the processing of nociception have led to renewed clinical interest in ketamine, an antagonist of the NMDA receptor. Low-dose ketamine had been reported to possess an analgesic effect though the paucity and inconsistency of such data have called for direct evaluation of this claim. This study, therefore, explored the analgesic effect of a sub-psychotomimetic dose of ketamine (SPDK), evaluated such effect on morphine- and diclofenac-induced analgesia, and determined its possible neuronal mechanism of analgesia. Mice weighing between 18-25 g were randomly distributed into two major groups consisting of Group 1 and 2 which were used for the assessment of analgesic effect and determination of the neuronal mechanism of 1 mg/kg ketamine using the hot plate model; and the formalin-induced pain model respectively. Data were presented as mean ± standard error of mean SEM and analyzed using ANOVA followed by post-hoc analysis (Student-Newman-Keuls) and P < 0.05 was set as an acceptable level of significance. The SPDK induced significant analgesia in the hot plate model but caused allodynia in the formalin-induced pain model. In addition, SPDK potentiated morphine-induced and diclofenac-induced analgesia in both the hot plate and formalin tests, while naloxone significantly blocked its analgesic effect at 90 minutes post-administration in the hot plate test. This study showed that SPDK induced analgesia in the acute pain model but aggravated pain in the chronic model. It also potentiated both morphine and diclofenac-induced analgesia possibly mediated through modulation of opioidergic pathway in mice.
Keywords: Sub-Psychotomimetic Dose, Ketamine, morphine, diclofenac, allodynia, hot plate model, formalin-induced pain model, NMDA receptors, opioidergic pathway
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Research Subject Categories::PHARMACY::Pharmaceutical pharmacology
Citation
Atunwa et al., 2017