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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Brain region-specific mechanisms for acute morphine-induced mitogen-activated protein kinase modulation and distinct patterns of activation during analgesic tolerance and locomotor sensitization.
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Brain region-specific mechanisms for acute morphine-induced mitogen-activated protein kinase modulation and distinct patterns of activation during analgesic tolerance and locomotor sensitization.

机译：急性吗啡诱导的丝裂原激活的蛋白激酶调节和止痛耐受性和运动敏化过程中的不同激活模式的大脑区域特定机制。

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Opioid-receptor activation in cell lines results in phosphorylation of p42/44 mitogen-activated protein kinase (MAPK), which contributes to agonist-induced desensitization of adenylate cyclase signaling. In this study, morphine-induced MAPK modulation was examined in the mouse brain using antibodies against phosphorylated MAPK. Thirty minutes after systemic morphine, MAPK modulation was observed in brain areas associated with analgesia and reward. Activation of MAPK was increased in the anterior cingulate (Acc), somato-sensory and association cortices, and locus ceruleus (LC). In contrast, MAPK activation was decreased in the nucleus accumbens and central amygdala (CeA). Double-label confocal microscopy revealed that morphine-induced MAPK modulation occurred predominantly in cells not expressing mu-opioid receptors, with the exception of the LC. Furthermore, the NMDA receptor antagonist 3,3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonate blocked morphine-induced MAPK modulation in several cortical areas including the Acc. We then examined morphine-induced MAPK modulation during expression of either analgesic tolerance or locomotor sensitization, which were differentiated by two repeated morphine regimens. Analgesic tolerance was accompanied by tolerance to morphine-induced MAPK modulation in all of the brain areas examined except the CeA. Locomotor sensitization resulted in sensitization to morphine-induced MAPK activation in the posterior basolateral amygdala. Additionally, a pronounced instatement of morphine-induced MAPK activation was observed in CA3 hippocampal processes. This instatement was observed during expression of tolerance; however, it was not significant during sensitization. In summary, these results provide distinct, region-specific mechanisms for morphine-induced MAPK modulation in the mouse brain and give insight into the brain circuitry involved in acute and adaptive opioid behaviors.
机译：细胞系中的阿片受体激活导致p42 / 44丝裂原活化蛋白激酶（MAPK）磷酸化，这有助于激动剂引起的腺苷酸环化酶信号转导的脱敏。在这项研究中，使用针对磷酸化MAPK的抗体在小鼠大脑中检测了吗啡诱导的MAPK调节。全身性吗啡注射后30分钟，在与镇痛和奖励有关的大脑区域观察到MAPK调节。在前扣带回（Acc），体感和联想皮层以及蓝斑（LC）中，MAPK的激活增加。相反，伏隔核和中央杏仁核（CeA）中的MAPK激活降低。双标记共聚焦显微镜显示，除了LC外，吗啡诱导的MAPK调节主要发生在不表达μ阿片受体的细胞中。此外，NMDA受体拮抗剂3,3-（2-羧基哌嗪-4-基）-丙基-1-膦酸酯在包括Acc在内的多个皮质区域阻断了吗啡诱导的MAPK调节。然后，我们在镇痛耐受性或运动敏化的表达过程中检查了吗啡诱导的MAPK调节，这通过两次重复的吗啡治疗方案来区分。除CeA以外，在所有检查的脑区域中，止痛耐受性均伴随对吗啡诱导的MAPK调节的耐受性。运动敏化导致对后基底外侧杏仁核中吗啡诱导的MAPK活化的敏化。此外，在CA3海马过程中观察到明显的吗啡诱导的MAPK活化。在宽容的表达过程中观察到这种陈述。然而，在敏化过程中它并不重要。总而言之，这些结果为小鼠脑中吗啡诱导的MAPK调节提供了独特的，区域特定的机制，并深入了解了参与急性和适应性阿片类药物行为的脑电路。

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