Interplay of cannabinoid 2 (CB2) receptors with nitric oxide synthases, oxidative and nitrative stress, and cell death during remote neurodegeneration

被引:22
|
作者
Pacher, Pal [1 ]
Mackie, Ken [2 ]
机构
[1] NIAAA, Sect Oxidat Stress Tissue Injury, Lab Physiol Studies, NIH, Bethesda, MD 20892 USA
[2] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN USA
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2012年 / 90卷 / 04期
关键词
Nitric Oxide; Traumatic Brain Injury; Amyotrophic Lateral Sclerosis; Peroxynitrite; Peripheral Nerve Injury;
D O I
10.1007/s00109-012-0884-1
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Remote neuronal degeneration and death/injury, which often occur in regions remote but functionally connected to the primary lesion site, may play a pivotal role in extending neuronal damage/dysfunction following traumatic brain injury, stroke, or peripheral nerve injury, as well as in chronic neurodegenerative diseases such as multiple sclerosis and amyotrophic lateral sclerosis. Even though the precise mechanisms of remote neuronal injury are poorly understood and no efficacious treatment options are available, it involves glial activation, inflammation, oxidative/nitrative stress, and apoptotic cell death. The newly discovered endocannabinoid signaling system consisting of endocannabinoids (endogenous bioactive lipid mediators), their synthetic and metabolizing enzymes, and their primary G protein-coupled cannabinoid 1 and 2 (CB1 and CB2) receptors has been implicated in the regulation of numerous physiological and pathological processes/functions, including those associated with neurodegeneration. Using a well-characterized rodent model of remote neuronal degeneration, Oddi et al. (J Mol Med 2012, in press, DOI 10.1007/s00109-012-0884-1) have demonstrated that targeting CB2 cannabinoid receptors may represent a promising novel approach to attenuate this pathological process. This editorial discusses the clinical significance of these interesting observations and the mechanisms of the possible interplay of CB2 receptors with nitric oxide synthases, oxidative and nitrative stress, and cell death during remote neurodegeneration.
引用
收藏
页码:347 / 351
页数:5
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