PMID- 28826541
OWN - NLM
STAT- MEDLINE
DCOM- 20171218
LR  - 20181202
IS  - 1557-8925 (Electronic)
IS  - 1054-3589 (Linking)
VI  - 80
DP  - 2017
TI  - Is the Cannabinoid CB(2) Receptor a Major Regulator of the Neuroinflammatory Axis 
      of the Neurovascular Unit in Humans?
PG  - 367-396
LID - S1054-3589(17)30037-6 [pii]
LID - 10.1016/bs.apha.2017.03.009 [doi]
AB  - The central nervous system (CNS) is an immune privileged site where the 
      neurovascular unit (NVU) and the blood-brain barrier (BBB) act as a selectively 
      permeable interface to control the passage of nutrients and inflammatory cells 
      into the brain parenchyma. However, in response to injury, infection, or disease, 
      CNS cells become activated, and release inflammatory mediators to recruit immune 
      cells to the site of inflammation. Increasing evidence suggests that cannabinoids 
      may have a neuroprotective role in CNS inflammatory conditions. For many years, 
      it was widely accepted that cannabinoid receptor type 1 (CB(1)) modulates 
      neurological function centrally, while peripheral cannabinoid receptor type 2 
      (CB(2)) modulates immune function. As knowledge about the physiology and 
      pharmacology of the endocannabinoid system advances, there is increasing interest 
      in targeting CB(2) as a potential treatment for inflammation-dependent CNS 
      diseases (Ashton & Glass, 2007), where recent rodent and human studies have 
      implicated intervention at the level of the NVU and BBB. These are incredibly 
      important in brain health and disease. Therefore, this review begins by 
      explaining the cellular and molecular components of these systems, highlighting 
      important molecules potentially regulated by cannabinoid ligands and then takes 
      an unbiased look at the evidence in support (or otherwise) of cannabinoid 
      receptor expression and control of the NVU and BBB function in humans.
CI  - (c) 2017 Elsevier Inc. All rights reserved.
FAU - Kho, Dan T
AU  - Kho DT
AD  - School of Medical Sciences, Faculty of Medical and Health Sciences, University of 
      Auckland, Auckland, New Zealand.
FAU - Glass, Michelle
AU  - Glass M
AD  - Faculty of Medical and Health Sciences, University of Auckland, Auckland, New 
      Zealand.
FAU - Graham, Euan S
AU  - Graham ES
AD  - School of Medical Sciences, Faculty of Medical and Health Sciences, University of 
      Auckland, Auckland, New Zealand. Electronic address: s.graham@auckland.ac.nz.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170612
PL  - United States
TA  - Adv Pharmacol
JT  - Advances in pharmacology (San Diego, Calif.)
JID - 9015397
RN  - 0 (Cannabinoids)
RN  - 0 (Receptor, Cannabinoid, CB2)
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/metabolism
MH  - Brain/*blood supply/metabolism/*pathology
MH  - Cannabinoids/metabolism
MH  - Humans
MH  - Inflammation/metabolism/*pathology
MH  - Models, Neurological
MH  - Receptor, Cannabinoid, CB2/*metabolism
OTO - NOTNLM
OT  - Blood-brain barrier
OT  - Brain
OT  - Cannabinoid
OT  - Cytokines
OT  - Inflammation
OT  - Leukocyte
OT  - Migration
OT  - Neuroinflammation
OT  - Neurovascular unit
OT  - Vascular
EDAT- 2017/08/23 06:00
MHDA- 2017/12/19 06:00
CRDT- 2017/08/23 06:00
PHST- 2017/08/23 06:00 [entrez]
PHST- 2017/08/23 06:00 [pubmed]
PHST- 2017/12/19 06:00 [medline]
AID - S1054-3589(17)30037-6 [pii]
AID - 10.1016/bs.apha.2017.03.009 [doi]
PST - ppublish
SO  - Adv Pharmacol. 2017;80:367-396. doi: 10.1016/bs.apha.2017.03.009. Epub 2017 Jun 
      12.