XXXX and @entity2227 released via astroglial @entity495 hemichannels mediate neuronal death through activation of @entity23656 hemichannels.

@entity1 @entity32 @entity2227 @entity6 @entity495 @entity310 @entity1356 @entity63 @entity2359 @entity519 @entity143 @entity23656 @entity195 @entity528 @entity413 @entity855
@entity32 contributes to neurodegeneration in post-ischemic brain, @entity6 , and @entity195 . @entity1 in this inflammatory response include activation of microglia and astrocytes. We studied the role of microglia treated with amyloid-b peptide (Ab) on hemichannel activity of astrocytes subjected to @entity519 in high @entity413 . Reoxygenation after 3   h @entity519 in high @entity413 induced transient astroglial permeabilization via @entity495 hemichannels and reduction in intercellular communication via @entity495 cell-cell channels. Both responses were greater and longer lasting in astrocytes previously exposed for 24 h to conditioned medium from Ab-treated microglia (CM-Ab). The effects of CM-Ab were mimicked by @entity310 and @entity1356 and were abrogated by neutralizing @entity310 with soluble receptor and @entity1356 with a receptor antagonist. Astrocytes under basal conditions protected neurons against @entity519 , but exposure to CM-Ab made them toxic to neurons subjected to a sub-lethal @entity519 /reoxygenation episode, revealing the additive nature of the insults. Astrocytes exposed to CM-Ab induced permeabilization of cortical neurons through activation of neuronal @entity23656 ( @entity23656 ) hemichannels by @entity855 and @entity2227 released through astroglial @entity495 hemichannels. In agreement, inhibition of @entity143 or P2X receptors only partially reduced the activation of neuronal @entity23656 hemichannels and neuronal mortality, but simultaneous inhibition of both receptors completely prevented the @entity2359 response. Therefore, we suggest that responses to @entity855 and @entity2227 converge in activation of neuronal @entity23656 hemichannels. Thus, we propose that blocking hemichannels expressed by astrocytes and/or neurons in the inflamed nervous system could represent a novel and alternative strategy to reduce @entity528 in various pathological states including @entity195 , @entity6 and @entity63 .
