Abstract
Transductional studies have suggested that the P2Y receptor signaling to the nucleus occurs through an early release of AA and induction of the fos and jun gene products, likely via the PKC/MAPK pathway or through a yet-to-be determined intracellular pathway involving products of arachidonate metabolism. Formation of Fos and Jun heterodimers upon challenge of astroglial cells with ATP has been suggested by Neary; these complexes may affect the transcription of genes specifically involved in the gliotic reaction. A new field concerns the identification of the molecules that specifically contribute to purine-induced reactive astrogliosis and it is anticipated that in the next few years several researchers will focus their attention on this intriguing topic. The finding that ATP has a role in reactive astrogliosis may also disclose novel therapeutic approaches to the modulation of post-traumatic and post-ischemic brain repair. In particular, recent data demonstrating induction of COX-2 in astrocytes upon stimulation of the gliotic P2Y receptor (Brambilla et al.,) may have intriguing implications in the therapy of neurological disorders characterized by excessive astroglial reaction and inflammation.