The effects of μ opioid receptors activation in mPFC and inactivation of Dopaminergic receptors in BLA during reference memory processing based on RAM test

Background and Aim : Spatial memories, including reference and working memory, are aspects of cognitive processes that examine human and animal abilities . Reference memory information can be changed according to circumstances. The hippocampus, as one of the main centers of memory processing and learning , modulates this type of memory through bilateral communication with the Amygdala and Prefrontal cortex. The present study investigated the role of μ opioid receptors in the medial Prefrontal cortex after blocking dopamine receptors in the Basolateral Amygdala.Methods : : Male Wistar rats were divided into twelve groups of six. After stereotaxic surgery and cannulation at the mPFC and BLA sites, mice underwent a 7-day recovery period. They then went on a 2hour daily diet according to the Watson and Packard protocol to reach 85% of their normal weight. Morphine as a μ opioid receptor agonist was injected to the mPFC at doses (0.5, 1 and 2 μl / rat) and Chlorpromazine as a dopamine antagonist at doses (0.5, 1 and 2 μl / rat) to the BLA on test day. Then the memory function of each rat was measured separately using an 8-arm radial maze.Results : High dose injection of Morphine and Chlorpromazine, by reducing reference memory error improved it P 0 / 05. But no change in the amount of time spent on the reference memory arm was seen P> 0/05. Co-administration of the effective dose of Morphine (2 l / rat) and triple doses of Chlorpromazine did not indicate a synergistic effect on reference memory P> 0.05, but also the results of the 2-way ANOVA analysis showed that compared to the groups receiving the Chlorpromazine dose alone, the reference memory error in this group Increased P 0/05 which indicates damage to the reference memory.Conclusion : Studies show that μ opioid and dopamine receptors are present in the same neurons in the brain cortex, suggesting close links between these two systems. Much of the rewarding effects of Morphine on memory behaviors are due to their effects on dopamine release. Chlorpromazine increases dopamine concentrations by inhibiting dopamine receptors. Previous studies have found high levels of dopamine prevent glutamate uptake. Thus, the excitability of neurons containing glutamate receptors in the Amygdala increases. Part of the effects of these two drugs appear to be through the activation of such pathways. Also Activation or inactivation of dopamine receptors in the BLA, alters the ratio of kinases to phosphatases, and vice versa, altering the activity of kinases and phosphatases, activates or deactivates different receptors. Given the above, it can be concluded that the effects of activation of μ opioid receptors or deactivation of dopamine receptors in the BLA on reference memory probably depend on at least a few factors. These effects are strongly dose dependent. The frequency of these receptors may influence their role in reference memory processing and Activation of them initiate completely different intracellular signaling pathways that can stimulate or inhibit neuronal activity.

کلیدواژه ها:

Reference memory ، mPFC ، BLA ، morphine ، chlorpromazine