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Hospital de Órbigo, Spain

Molina-Holgado E.,Laboratorio Of Neuroinflamacion | Molina-Holgado F.,Roehampton University
Journal of Neurochemistry | Year: 2010

Neuroimmune networks and the brain endocannabinoid system contribute to the maintenance of neurogenesis. Cytokines and chemokines are important neuroinflammatory mediators that are involved in the pathological processes resulting from brain trauma, ischemia and chronic neurodegenerative diseases. However, they are also involved in brain repair and recovery. Compelling evidence obtained, in vivo and in vitro, establish a dynamic interplay between the endocannabinoid system, the immune system and neural stem/progenitor cells (NSC) in order to promote brain self-repair. Cross-talk between inflammatory mediators and NSC might have important consequences for neural development and brain repair. In addition, brain immune cells (microglia) support NSC renewal, migration and lineage specification. The proliferation and differentiation of multipotent NSC must be precisely controlled during the development of the CNS, as well as for adult brain repair. Although signalling through neuroimmune networks has been implicated in many aspects of neural development, how it affects NSC remains unclear. However, recent findings have clearly demonstrated that there is bi-directional cross-talk between NSC, and the neuroimmune network to control the signals involved in self-renewal and differentiation of NSC. Specifically, there is evidence emerging that neuroimmune interactions control the generation of new functional neurones from adult NSC. Here, we review the evidence that neuroimmune networks contribute to neurogenesis, focusing on the regulatory mechanisms that favour the immune system (immune cells and immune molecules) as a novel element in the coordination of the self-renewal, migration and differentiation of NSC in the CNS. In conjunction, these data suggest a novel mode of action for the immune system in neurogenesis that may be of therapeutic interest in the emerging field of brain repair. © 2010 International Society for Neurochemistry. Source


Garcia-Ovejero D.,Laboratorio Of Neuroinflamacion | Gonzalez S.,Institute Biologia y Medicina Experimental | Gonzalez S.,University of Buenos Aires | Paniagua-Torija B.,Laboratorio Of Neuroinflamacion | And 6 more authors.
Journal of Neurotrauma | Year: 2014

Progesterone is an anti-inflammatory and promyelinating agent after spinal cord injury, but its effectiveness on functional recovery is still controversial. In the current study, we tested the effects of chronic progesterone administration on tissue preservation and functional recovery in a clinically relevant model of spinal cord lesion (thoracic contusion). Using magnetic resonance imaging, we observed that progesterone reduced both volume and rostrocaudal extension of the lesion at 60 days post-injury. In addition, progesterone increased the number of total mature oligodendrocytes, myelin basic protein immunoreactivity, and the number of axonal profiles at the epicenter of the lesion. Further, progesterone treatment significantly improved motor outcome as assessed using the Basso-Bresnahan-Beattie scale for locomotion and CatWalk gait analysis. These data suggest that progesterone could be considered a promising therapeutical candidate for spinal cord injury. © 2014 Mary Ann Liebert, Inc. Source


Arevalo-Martin A.,Laboratorio Of Neuroinflamacion | Garcia-Ovejero D.,Laboratorio Of Neuroinflamacion | Sierra-Palomares Y.,Laboratorio Of Neuroinflamacion | Paniagua-Torija B.,Laboratorio Of Neuroinflamacion | And 3 more authors.
PLoS ONE | Year: 2012

Spinal cord injury (SCI) induces a cascade of processes that may further expand the damage (secondary injury) or, alternatively, may be part of a safeguard response. Here we show that after a moderate-severe contusive SCI in rats there is a significant and very early increase in the spinal cord content of the endocannabinoids 2-arachidonoylglycerol (2-AG) and arachidonoyl ethanolamide (anandamide, AEA). Since 2-AG and AEA act through CB1 and CB2 cannabinoid receptors, we administered at 20 minutes after lesion a single injection of their respective antagonists AM281 and AM630 alone or in combination to block the effects of this early endocannabinoid accumulation. We observed that AM281, AM630 or AM281 plus AM630 administration impairs the spontaneous motor recovery of rats according to the Basso-Beattie-Bresnahan (BBB) locomotor scale. However, blockade of CB1, CB2 or both receptors produced different effects at the histopathological level. Thus, AM630 administration results at 90 days after lesion in increased MHC-II expression by spinal cord microglia/monocytes and reduced number of serotoninergic fibres in lumbar spinal cord (below the lesion). AM281 exerted the same effects but also increased oedema volume estimated by MRI. Co-administration of AM281 and AM630 produced the effects observed with the administration of either AM281 or AM630 and also reduced white matter and myelin preservation and enhanced microgliosis in the epicentre. Overall, our results suggest that the endocannabinoids acting through CB1 and CB2 receptors are part of an early neuroprotective response triggered after SCI that is involved in the spontaneous recovery after an incomplete lesion. © 2012 Arevalo-Martin et al. Source

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