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Abstract:
Pharmacological agents limiting secondary tissue loss and improving functional outcomes after stroke are still limited. Cannabidiol (CBD), the major non-psychoactive component of
Cannabis sativa, has been proposed as a neuroprotective agent against experimental cerebral ischemia.
The effects of CBD mostly relate to the modulation of neuroinflammation, including glial activation.
To investigate the effects of CBD on glial cells after focal ischemia in vivo, we performed time-lapse
imaging of microglia and astroglial Ca2+ signaling in the somatosensory cortex in the subacute phase
of stroke by in vivo two-photon laser-scanning microscopy using transgenic mice with microglial
EGFP expression and astrocyte-specific expression of the genetically encoded Ca2+ sensor GCaMP3.
CBD (10 mg/kg, intraperitoneally) prevented ischemia-induced neurological impairment, reducing
the neurological deficit score from 2.0 ± 1.2 to 0.8 ± 0.8, and protected against neurodegeneration,
as shown by the reduction (more than 70%) in Fluoro-Jade C staining (18.8 ± 7.5 to 5.3 ± 0.3).
CBD reduced ischemia-induced microglial activation assessed by changes in soma area and total
branch length, and exerted a balancing effect on astroglial Ca2+ signals. Our findings indicate that
the neuroprotective effects of CBD may occur in the subacute phase of ischemia, and reinforce its
strong anti-inflammatory property. Nevertheless, its mechanism of action on glial cells still requires
further studies
