Porcine pancreatic group IB secretory phospholipase A2 potentiates XXXX influx through L-type voltage-sensitive @entity141 channels.

@entity141 @entity460 @entity35 @entity25191 @entity2359
Secretory phospholipase A(2) ( @entity25191 ) exhibits @entity2359 in the central nervous system. There are high-affinity binding sites of the porcine pancreatic group IB @entity25191 ( @entity25191 ) in the brain. @entity25191 causes neuronal cell death via apoptosis in the @entity35 cerebral cortex. Although apoptosis is triggered by an influx of @entity141 into neurons, it has not yet been ascertained whether the @entity141 influx is associated with the @entity2359 of @entity25191 . We thus examined the possible involvement of @entity141 in the @entity2359 of @entity25191 in the primary culture of @entity35 cortical neurons. @entity25191 induced neuronal cell death in a concentration- and time-dependent manner. This death was accompanied by condensed chromatin and fragmented DNA, exhibiting apoptotic features. Before apoptosis, @entity25191 markedly enhanced the influx of @entity141 into neurons. A @entity460 chelator suppressed neurons from @entity25191 -induced neuronal cell death in a concentration-dependent manner. An L-type voltage-sensitive @entity141 channel (L-VSCC) blocker significantly protected the @entity25191 -potentiated influx of @entity141 . On the other hand, blockers of N-VSCC and P/Q-VSCC did not. An L-VSCC blocker protected neurons from @entity25191 -induced neuronal cell death. In addition, the L-VSCC blocker ameliorated the apoptotic features of @entity25191 -treated neurons. Neither an N-VSCC blocker nor P/Q-VSCC blockers affected the @entity2359 of the enzyme. In conclusion, these findings demonstrate that the influx of @entity141 into neurons play an important role in the @entity2359 of @entity25191 . Furthermore, the present study suggests that L-VSCC contribute to the @entity25191 -potentiated influx of @entity141 into neurons.
