Person: Ceprián Costoso, María
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Caracterización de los efectos neuroprotectores del cannabidiol en el daño cerebral hipóxico-isquémico neonatal
El daño hipóxico-‐isquémico (HI) neonatal es una patología grave cuya principal secuela es la parálisis cerebral. Dos de las principales patologías HI neonatales son la Encefalopatía Hipóxico-‐Isquémica Neonatal (NHIE)1, caracterizado por un daño cerebral global y difuso, y el Infarto Isquémico Arterial Perinatal (PAIS), un daño HI focal que afecta principalmente al territorio dela arteria cerebral media izquierda.El origen del daño HI es el descenso de glucosa y oxígeno causado por la disminución del flujo cerebral, que induce la llamada “triada mortal” (excitotoxicidad, estrés oxidativo e inflamación),que conduce a la muerte celular y al daño cerebral. Al ser los oligodendrocitos, especialmente en su etapa de pre-‐oligodendrocitos, especialmente sensibles al daño la HI produce una hipomielinización. Los astrocitos y la microglia promueven activamente la “triada mortal “ pero también son fundamentales en la respuesta reparativa generada por la HI...
Glial Cell AMPA Receptors in Nervous System Health, Injury and Disease
Glia form a central component of the nervous system whose varied activities sustain an environment that is optimised for healthy development and neuronal function. Alpha-amino-3-hydroxy-5-methyl-4-isoxazole (AMPA)-type glutamate receptors (AMPAR) are a central mediator of glutamatergic excitatory synaptic transmission, yet they are also expressed in a wide range of glial cells where they influence a variety of important cellular functions. AMPAR enable glial cells to sense the activity of neighbouring axons and synapses, and as such many aspects of glial cell development and function are influenced by the activity of neural circuits. However, these AMPAR also render glia sensitive to elevations of the extracellular concentration of glutamate, which are associated with a broad range of pathological conditions. Excessive activation of AMPAR under these conditions may induce excitotoxic injury in glial cells, and trigger pathophysiological responses threatening other neural cells and amplifying ongoing disease processes. The aim of this review is to gather information on AMPAR function from across the broad diversity of glial cells, identify their contribution to pathophysiological processes, and highlight new areas of research whose progress may increase our understanding of nervous system dysfunction and disease.