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By sustained activation of opioid receptors, chronic opioids cause analgesic tolerance, physical dependence, and opioid addiction, for which an effective treatment is still lacking.Amygdala, as a part of limbic system, plays an important role in opioid addiction.In this study, we using patch clamp recording method combined with pharmacological approaches investigated chronic morphine-induced adaptations in glutamatergic synaptic transmission in neurons of the basolateral amygdala (BLA).Chronic morphine significantly increased glutamate synaptic transmission in pyramidal neurons in BLA containingμ-opioid receptors.In naive rats, DAMGO,μ-opioid receptors activator, could inhibit the release ofpresynaptic glutamate, while DAMGO would lost this inhibitory effect in chronic morphine group.We found that in saline rats, DAMGOs effect was blocked by AACOCF3, an inhibitor of phospholipase A2 and 4-AP, which blocks the presynaptic voltage-dependent potassium channels regulated by metabolites of the PLA2 pathway.But PKA didnt play any roles in na(i)ye group.Next, we confirmed that in chronic morphine group, PLA2-AA-Kv pathway was downregulated and PKA was upregulated, which were involved in the effect of DAMGO on presynaptic glutamate release.Our job provided the new mechanism of opioid receptors in morphine treatment for further clinical perspective.