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2010 ; 226
(1
): 231-41
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A synthetic cannabinoid agonist promotes oligodendrogliogenesis during viral
encephalitis in rats
#MMPMID20832403
Solbrig MV
; Fan Y
; Hermanowicz N
; Morgese MG
; Giuffrida A
Exp Neurol
2010[Nov]; 226
(1
): 231-41
PMID20832403
show ga
Chronic CNS infection by several families of viruses can produce deficits in
prefrontal cortex (PFC) and striatal function. Cannabinoid drugs have been long
known for their anti-inflammatory properties and their ability to modulate adult
neuro and gliogenesis. Therefore, we explored the effects of systemic
administration of the cannabinoid agonist WIN55,212-2(WIN) on prefrontal cortex
(PFC) and striatal cytogenesis in a viral model of CNS injury and inflammation
based on Borna Disease (BD) virus encephalitis. Active BrdU(+) progenitor
populations were significantly decreased 1 week after BrdU labeling in BD rats
[p<0.001 compared to uninfected (NL) controls] while less than 5% of BrdU(+)
cells colabeled for BDV protein. Systemic WIN (1mg/kg i.p. twice daily×7 days)
increased the survival of BrdU(+) cells in striatum (p<0.001) and PFC of BD rats,
with differential regulation of labeled oligodendroglia precursors vs
microglia/macrophages. WIN increased the percentage of BrdU(+) oligodendrocyte
precursor cells and decreased BrdU(+) ED-1-labeled phagocytic cells, without
producing pro- or antiviral effects. BDV infection decreased the levels of the
endocannabinoid anandamide (AEA) in striatum (p<0.05 compared to NL rats),
whereas 2-AG levels were unchanged. Our findings indicate that: 1) viral
infection is accompanied by alterations of AEA transmission in the striatum, but
new cell protection by WIN appears independent of its effect on endocannabinoid
levels; and 2) chronic WIN treatment alters the gliogenic cascades associated
with CNS injury, promoting oligodendrocyte survival. Limiting reactive
gliogenesis and macrophage activity in favor of oliogodendroglia development has
significance for demyelinating diseases. Moreover, the ability of cannabinoids to
promote the development of biologically supportive or symbiotic oligodendroglia
may generalize to other microglia-driven neurodegenerative syndromes including
NeuroAIDS and diseases of aging.