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Cannabinoids modulate Olig2 and polysialylated neural cell adhesion molecule expression in the subventricular zone of post‐natal rats through cannabinoid receptor 1 and cannabinoid receptor 2
Author(s) -
ArévaloMartín Ángel,
GarcíaOvejero Daniel,
RubioAraiz Ana,
Gómez Oscar,
MolinaHolgado Francisco,
MolinaHolgado Eduardo
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05782.x
Subject(s) - subventricular zone , cannabinoid receptor , cannabinoid , olig2 , neural cell adhesion molecule , cannabinoid receptor type 2 , neuroscience , microbiology and biotechnology , astrocyte , cell adhesion molecule , myelin , receptor , biology , chemistry , neural stem cell , oligodendrocyte , cell adhesion , agonist , cell , central nervous system , stem cell , biochemistry
The subventricular zone (SVZ) is a source of post‐natal glial precursors that can migrate to the overlying white matter, where they may differentiate into oligodendrocytes. We showed that, in the post‐natal SVZ ependymocytes, radial glia and astrocyte‐like cells express cannabinoid receptor 1 (CB1), whereas cannabinoid receptor 2 (CB2) is found in cells expressing the polysialylated neural cell adhesion molecule. To study CB1 and CB2 function, post‐natal rats were exposed to selective CB1 or CB2 agonists (arachidonyl‐2‐chloroethylamide and JWH‐056, respectively) for 15 days. Accordingly, we found that CB1 activation increases the number of Olig2‐positive cells in the dorsolateral SVZ, whereas CB2 activation increases polysialylated neural cell adhesion molecule expression in this region. As intense myelination occurs during the first weeks of post‐natal development, we examined how modulating these factors affected the expression of myelin basic protein. Pharmacological administration of agonists and antagonists of CB1 and CB2 showed that the activation of both receptors is needed to augment the expression of myelin basic protein in the subcortical white matter.