L. Mititelu-Tarțău, M. Bogdan, V. Gheorman, L. Foia, Ancuța Goriuc, G. Rusu, B. R. Buca, L. Pavel, A. Cristofor, C. Tartau, G. Popa
{"title":"Current Therapeutic Approaches from Imidazoline and Opioid Receptors Modulators in Neuroprotection","authors":"L. Mititelu-Tarțău, M. Bogdan, V. Gheorman, L. Foia, Ancuța Goriuc, G. Rusu, B. R. Buca, L. Pavel, A. Cristofor, C. Tartau, G. Popa","doi":"10.5772/INTECHOPEN.81951","DOIUrl":null,"url":null,"abstract":"Due to brain plasticity, the nervous system is capable of manifesting behavioral variations, adapted to the influences from both external and internal environment. Multiple neurotransmitters are involved in the mediation of pathological processes at the molecular, cellular, regional, and interregional levels participating in cerebral plasticity, their intervention being responsible for various structural, functional, and behavioral disturbances. The current therapeutic strategies in neuroprotection aim at blocking on different levels, the molecular cascades of the pathophysiological mechanisms responsible for neuronal dysfunctions and ultimately for neuronal death. Different agents influencing these neurotransmitters have demonstrated beneficial effects in neurogenesis and neuroprotection, proved in experimental animal models of focal and global ischemic injuries. Serotonin, dopamine, glutamate, N-methyl-D-aspartate, and nitric oxide have been shown to play a significant role in modulating nervous system injuries. The imidazoline system is one of the important systems involved in human brain functioning. Experimental investigations have revealed the cytoprotective effects of imidazoline I2 receptor ligands against neuronal injury induced by hypoxia in experimental animals. The neuroprotective effects were also highlighted for kappa and delta receptors, whose agonists demonstrated the ability to reduce architectural lesions and to recover neuronal functions of animals with experimentally induced brain ischemia.","PeriodicalId":74291,"journal":{"name":"Neuroprotection","volume":"28 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroprotection","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.81951","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Due to brain plasticity, the nervous system is capable of manifesting behavioral variations, adapted to the influences from both external and internal environment. Multiple neurotransmitters are involved in the mediation of pathological processes at the molecular, cellular, regional, and interregional levels participating in cerebral plasticity, their intervention being responsible for various structural, functional, and behavioral disturbances. The current therapeutic strategies in neuroprotection aim at blocking on different levels, the molecular cascades of the pathophysiological mechanisms responsible for neuronal dysfunctions and ultimately for neuronal death. Different agents influencing these neurotransmitters have demonstrated beneficial effects in neurogenesis and neuroprotection, proved in experimental animal models of focal and global ischemic injuries. Serotonin, dopamine, glutamate, N-methyl-D-aspartate, and nitric oxide have been shown to play a significant role in modulating nervous system injuries. The imidazoline system is one of the important systems involved in human brain functioning. Experimental investigations have revealed the cytoprotective effects of imidazoline I2 receptor ligands against neuronal injury induced by hypoxia in experimental animals. The neuroprotective effects were also highlighted for kappa and delta receptors, whose agonists demonstrated the ability to reduce architectural lesions and to recover neuronal functions of animals with experimentally induced brain ischemia.
由于大脑的可塑性,神经系统能够表现出行为变化,以适应外部和内部环境的影响。多种神经递质在参与大脑可塑性的分子、细胞、区域和区域间水平上参与病理过程的调解,它们的干预负责各种结构、功能和行为障碍。目前神经保护的治疗策略旨在不同水平上阻断导致神经元功能障碍并最终导致神经元死亡的病理生理机制的分子级联。在局灶性和全局性缺血性损伤的实验动物模型中,影响这些神经递质的不同药物已显示出对神经发生和神经保护的有益作用。血清素、多巴胺、谷氨酸、n -甲基- d -天冬氨酸和一氧化氮已被证明在调节神经系统损伤中发挥重要作用。咪唑啉系统是参与人脑功能的重要系统之一。实验研究发现咪唑啉I2受体配体对实验动物缺氧诱导的神经元损伤具有细胞保护作用。kappa和delta受体的神经保护作用也被强调,它们的激动剂显示出减少实验性脑缺血动物的结构损伤和恢复神经元功能的能力。