http://cercor.oxfordjournals.org/content/early/2013/08/19/cercor.bht202.abstract
- Ana Belen Lopez-Rodriguez1,5,
- Eleni Siopi2,
- David P. Finn4,
- Catherine Marchand-Leroux2,
- Luis M. Garcia-Segura5,
- Mehrnaz Jafarian-Tehrani2,3 and
- Maria-Paz Viveros1⇑
+ Author Affiliations
- Address correspondence to Maria-Paz Viveros, Department of Animal Physiology (Animal Physiology II), Faculty of Biology, Complutense University of Madrid, Calle Jose Antonio Novais 2, Madrid 28040, Spain. Email: pazviver@bio.ucm.es
Abstract
Traumatic brain injury (TBI) and its
consequences represent one of the leading causes of death in young
adults. This lesion
mediates glial activation and the release of
harmful molecules and causes brain edema, axonal injury, and functional
impairment.
Since glial activation plays a key role in the
development of this damage, it seems that controlling it could be
beneficial
and could lead to neuroprotective effects. Recent
studies show that minocycline suppresses microglial activation, reduces
the lesion volume, and decreases TBI-induced
locomotor hyperactivity up to 3 months. The endocannabinoid system (ECS)
plays
an important role in reparative mechanisms and
inflammation under pathological situations by controlling some
mechanisms that
are shared with minocycline pathways. We
hypothesized that the ECS could be involved in the neuroprotective
effects of minocycline.
To address this hypothesis, we used a murine TBI
model in combination with selective CB1 and CB2 receptor antagonists
(AM251
and AM630, respectively). The results provided the
first evidence for the involvement of ECS in the neuroprotective action
of minocycline on brain edema, neurological
impairment, diffuse axonal injury, and microglial activation, since all
these
effects were prevented by the CB1 and CB2 receptor
antagonists.
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