Brain platelet-activating factor (PAF) is a lipid mediator involved in neurotransmission and in LTP. It has been reported that the induction of LTP by high frequency stimulation increases the activity of the enzymes responsible for its synthesis by a still unknown mechanism (1). One of the two biosynthetic pathways is Ca2+-dependent and transforms a membrane ether phospholipid into PAF by a sequence of two reactions being the first one, catalyzed by a phospholipase A2 (PLA2), rate limiting. Overproduction of PAF, takingplaceinpathologicalconditions,contributestobraindamage. Various PLA2s are present in brain tissue and, particularly, sPLA2- IIA is very likely involved in the production of PAF as its expression increases in pathological conditions. Recently, we have foundthereleaseofsPLA2-IIAfromratbraincortexmitochondria and its association with nuclear membranes, which might be an intracellular target for the enzyme. Reference 1. Francescangeli E. et al. (2002) Neurochem. Res. 27, 1465–1471.
Platelet-activating factor: role in long-term potentiation and in brain damage
FRANCESCANGELI, Ermelinda;NARDICCHI, Vincenza;MACCHIONI, Lara;GORACCI, Gianfrancesco
2003
Abstract
Brain platelet-activating factor (PAF) is a lipid mediator involved in neurotransmission and in LTP. It has been reported that the induction of LTP by high frequency stimulation increases the activity of the enzymes responsible for its synthesis by a still unknown mechanism (1). One of the two biosynthetic pathways is Ca2+-dependent and transforms a membrane ether phospholipid into PAF by a sequence of two reactions being the first one, catalyzed by a phospholipase A2 (PLA2), rate limiting. Overproduction of PAF, takingplaceinpathologicalconditions,contributestobraindamage. Various PLA2s are present in brain tissue and, particularly, sPLA2- IIA is very likely involved in the production of PAF as its expression increases in pathological conditions. Recently, we have foundthereleaseofsPLA2-IIAfromratbraincortexmitochondria and its association with nuclear membranes, which might be an intracellular target for the enzyme. Reference 1. Francescangeli E. et al. (2002) Neurochem. Res. 27, 1465–1471.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
