UNASSIGNED: @entity63 is a multifactorial pathology characterized by different events evolving in the time. After @entity63 a @entity16 due to the early massive increase of extracellular @entity3264 is followed by activation of resident immune cells, i.e microglia, and production or activation of @entity32 mediators. Protracted neuroinflammation is now recognized as the predominant mechanism of secondary @entity1545 progression. Extracellular concentrations of @entity855 and @entity859 in the brain increase dramatically during @entity63 in concentrations able to stimulate their respective specific P2 and P1 receptors. Both @entity855 P2 and @entity859 P1 receptor subtypes exert important roles in @entity63 . Although @entity859 exerts a clear neuroprotective effect through A1 receptors during @entity63 , the use of selective A1 agonists is hampered by undesirable peripheral effects. Evidence up to now in literature indicate that A2A receptor antagonists provide protection centrally by reducing excitotoxicity, while agonists at A2A (and possibly also A2B) and A3 receptors provide protection by controlling massive infiltration and neuroinflammation in the hours and days after @entity2806 . Among P2X receptors most evidence indicate that @entity9896 contribute to the damage induced by the @entity63 insult due to intracellular @entity141 loading in central cells and facilitation of @entity3264 release. Antagonism of P2X7 receptors might represent a new treatment to attenuate @entity75 and to promote proliferation and maturation of brain immature resident cells that can promote tissue repair following @entity2806 . Among P2Y receptors, antagonists of @entity3075 receptors are of value because of their antiplatelet activity and possibly because of additional anti-inflammatory effects. Moreover strategies that modify @entity859 or @entity855 concentrations at injury sites might be of value to limit damage after @entity63 .

Purinergic signalling in XXXX .

@entity1545 :: ('MESH:D020214', 'Disease') :: ['brain injury'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity3264 :: ('D018698', 'Chemical') :: ['glutamate'] @entity859 :: ('MESH:D000241', 'Chemical') :: ['adenosine'] @entity2806 :: ('MESH:D002545', 'Disease') :: ['brain ischemia', 'cerebral ischemia'] @entity63 :: ('MESH:D007511', 'Disease') :: ['Ischemia', 'ischemia', 'ischemic'] @entity75 :: ('MESH:D001927', 'Disease') :: ['brain damage'] @entity16 :: ('MESH:D009422', 'Disease') :: ['primary damage'] @entity9896 :: ('5027', 'Gene') :: ['P2X7 receptor'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca(2+)'] @entity3075 :: ('64805', 'Gene') :: ['P2Y12'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity2806 :: (MESH:D002545,Disease) :: ['brain ischemia']
