Producción CyT
Artículo
Autoría
Gonzalez, Susana Laura
;
CORONEL, MARIA FLORENCIA
Fecha
2016
Editorial y Lugar de Edición
Medknow Publications
Revista
NEURAL REGENERATION RESEARCH,
vol. 11
(pp. 1238-1240)
Medknow Publications
Resumen
Información suministrada por el agente en
SIGEVA
Neuropathic pain, a type of pain arising after directdamage or disease of the nervous system, is often intractable and challengesthe search of effective therapeutic strategies. In particular, neuropathic painis a very frequent sequel of spinal cord injury (SCI) and a decisive contributor todecreased quality of life. Several and intricate mechanisms appear to be involvedin the onset and maintenance of neuropathic pain after SCI. However, it is onlywithin the last years that neuroinflammatory con...
Neuropathic pain, a type of pain arising after directdamage or disease of the nervous system, is often intractable and challengesthe search of effective therapeutic strategies. In particular, neuropathic painis a very frequent sequel of spinal cord injury (SCI) and a decisive contributor todecreased quality of life. Several and intricate mechanisms appear to be involvedin the onset and maintenance of neuropathic pain after SCI. However, it is onlywithin the last years that neuroinflammatory consequences of SCI have beenlinked to the stubborn pain that these patients may suffer (Walters, 2014). Neuroinflammationoccurs in the nervous system as a response to pathogens, toxins, trauma orneurodegeneration, and contemplates the active participation of glial cells.While a controlled neuroinflammatory response after injury has been shown toplay a neuroprotective role, dysregulation of glial cells - mainly microgliaand astrocytes - may result detrimental to neurons and other glial cells, viathe production of neurotoxic factors that exacerbate the damage. Inparticular, reactive gliosis along with the release ofpro-inflammatory cytokines is a signature of human and experimental centralnervous system (CNS) injury and is critically placed at the crossroads of neuroinflammation and neuropathicpain (Walters, 2014). However, a main concern after SCI is that generalsuppression of inflammation may impair regeneration and repair in the spinalcord. These concepts challenge the development of novel strategies aimed at reducing pain withoutinterfering with functional outcomes. Based upon an active research over the past decades,it is now a well-consolidated concept that progesterone, beyond its recognizedrole in reproduction, acts as a neurosteroid/neuroactive steroid with multipleand diverse functions in the nervous system (De Nicola et al., 2013). Thesefunctions, comprising neuroprotection, myelin formation, control of inflammation,regulation of glial cell function and neurotransmission,have been recentlyextended to the modulation of pain sensitivity (Coronel et al., 2011). In fact,progesterone,a well-known suppressor of the inflammatory response following CNSinjury, stands as a promising candidate to block the multiple cellular andmolecular events leading to damage and chronic pain after SCI (Garcia-Ovejero etal., 2014; Coronel et al., 2016).
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Palabras Clave
SPINAL CORD INJURYNEUROPATHIC PAINPROGESTERONE
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