Department of Pharmacology and Pharmacodynamics, Medical University of Lublin, Chodzki 4a St., 20-093 Lublin, Poland.
Int J Mol Sci. 2019 Sep 3;20(17):4302. doi: 10.3390/ijms20174302.
Opioid use disorder is classified as a chronic recurrent disease of the central nervous system (CNS) which leads to personality disorders, co-morbidities and premature death. It develops as a result of long-term administration of various abused substances, along with morphine. The pharmacological action of morphine is associated with its stimulation of opioid receptors. Opioid receptors are a group of G protein-coupled receptors and activation of these receptors by ligands induces significant molecular changes inside the cell, such as an inhibition of adenylate cyclase activity, activation of potassium channels and reductions of calcium conductance. Recent data indicate that other signalling pathways also may be involved in morphine activity. Among these are phospholipase C, mitogen-activated kinases (MAP kinases) or β-arrestin. The present review focuses on major mechanisms which currently are considered as essential in morphine activity and dependence and may be important for further studies.
阿片类药物使用障碍被归类为一种中枢神经系统(CNS)的慢性复发性疾病,导致人格障碍、合并症和过早死亡。它是由于长期使用各种滥用物质以及吗啡引起的。吗啡的药理学作用与其对阿片受体的刺激有关。阿片受体是一组 G 蛋白偶联受体,配体对这些受体的激活会在细胞内引起显著的分子变化,例如抑制腺苷酸环化酶活性、激活钾通道和降低钙电导。最近的数据表明,其他信号通路也可能参与吗啡的活性。其中包括磷脂酶 C、丝裂原激活的蛋白激酶(MAPK)或β-arrestin。本综述重点介绍了目前被认为是吗啡活性和依赖性的重要机制,并且可能对进一步的研究很重要。