The CB2 cannabinoid receptor as a therapeutic target in the central nervous system

2021 ◽  
Vol 25 (8) ◽  
pp. 659-676
Author(s):  
David Cabañero ◽  
Elena Martín-García ◽  
Rafael Maldonado
2021 ◽  
Vol 15 ◽  
Author(s):  
Lu Cao ◽  
Yanbo Zhou ◽  
Mengguang Chen ◽  
Li Li ◽  
Wei Zhang

Pericytes are perivascular multipotent cells located on capillaries. Although pericytes are discovered in the nineteenth century, recent studies have found that pericytes play an important role in maintaining the blood—brain barrier (BBB) and regulating the neurovascular system. In the neurovascular unit, pericytes perform their functions by coordinating the crosstalk between endothelial, glial, and neuronal cells. Dysfunction of pericytes can lead to a variety of diseases, including stroke and other neurological disorders. Recent studies have suggested that pericytes can serve as a therapeutic target in ischemic stroke. In this review, we first summarize the biology and functions of pericytes in the central nervous system. Then, we focus on the role of dysfunctional pericytes in the pathogenesis of ischemic stroke. Finally, we discuss new therapies for ischemic stroke based on targeting pericytes.


2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Guoqin Xu ◽  
Hong Zhao

Objective As we all know, exercise can enhance the will, improve the mood, and counteract the bad feelings of the body, but the cause and mechanism of action have not been clear. The endocannabinoid system is an important regulatory system in the central nervous system that regulates cognition, mood and behavior. Endocannabinoids can exert physiological regulation through cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2). Cannabinoid receptors are widely distributed in the body and participate in the regulation of anti-nociceptive signals at multiple levels. This study will explore the role and mechanism of the endocannabinoid system in exercise-induced antinociception by literature research methods. Methods Using endocannabinoid, exercise/sports and antinociception or emotion as keywords, using Pubmed, Medline, and Embase databases to search for nearly 15 years of research literature and the literatures from cross-references of journals, after excluding the literature that is not relevant to the research content, the 12 articles included were analyzed. Results Exercise can activate the endocannabinoid system, the degree of activation is related to exercise intensity, and high-intensity exercise significantly increases endocannabinoid levels in the human body. Cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2) are widely distributed in the nervous system including the central nervous system and the peripheral nervous system. When exercise activates the endocannabinoid system, the increased endocannabinoid in the circulatory system activates CB1 and CB2 receptors, promotes hyperpolarization of the nervous system cells, reduces the rate of excitable cell release, and inhibits neurotransmitters, and reduce nociceptive impulses, thereby the body produces anti-nociception. Pretreatment with endocannabinoid metabolic enzyme inhibitors (MAFP, JZL184) and endocannabinoid reuptake inhibitors (VDM11) can be extended and enhanced the antinociceptive effect of exercise. Pretreatment with endocannabinoid receptor antagonists (AM251 and AM630) will inhibit the antinociception induced by aerobic exercise in mechanical and thermal nociceptive tests. Conclusions Exercise can enhance the level of circulating endocannabinoids, activate the endocannabinoid system through endocannabinoid receptors, and then induce the body to produce anti-nociceptive effects. The degree of activation is related to exercise intensity. Studying the role and mechanism of the endocannabinoid system in exercise-induced antinociception can provide a theoretical basis for exercise to improve depression, anxiety and other emotions, improve the sense of life and prevent mental disorders.


2019 ◽  
Vol 1 (Supplement_2) ◽  
pp. ii8-ii8
Author(s):  
Seon-Jin Yoon ◽  
Junseong Park ◽  
Hyun Jung Kim ◽  
Joo Ho Lee ◽  
Jong Hee Chang ◽  
...  

Abstract Treatment of Glioblastoma (GBM), IDH-wildtype is a history of sequential failure. The cure for this disease is a distant story, and it is really the emperor of cancer. We believe that GBM should not be considered one of several cancers, and GBM is a cancer that occurs in a special environment called the central nervous system (CNS). What is the biggest difference between other cancers and cancers of the nervous system? It is thought to be neurogenesis. This presentation will review GBM genesis based on neurogensis of CNS. It also explains what the cell of origin is, what somatic mutations occur at the cell of origin, and why these somatic mutations occur. Human glioblastoma (GBM) occurs in a place without cancer tissue, that is, in the subventricular zone and have introduced the name of the firework pattern of cancer genesis, which is a metaphorical representation of the GBM genesis. So far, we have been trying to develop therapeutics focused on bulk tumors. However, in the case of GBM, IDH-wildtype, it has been found that the cell of origin is not in the tumor but is in normal SVZ, so it is now considered that the therapeutic target should also include the cell of origin.


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