Protein Kinase C is Partially responsible for the Effects of NF1 in Sustaining EPSP Amplitude Increase
We used crayfish neuromuscular preps to examine the role of protein kinases in general and Protein Kinase C (PKC) in particular in the effects of sustaining EPSP amplitude increases induced by NF1. We used intracellular recordings to measure changes in EPSP amplitudes over time under the effects of different protein kinase inhibitors and NF1 as compared to baseline measurements taken before the exposure to drugs/NF1. We found that preps exposed to NF1 experienced a sustained increase in EPSP amplitude relative to their baseline measurements. We also found that while preps exposed to NF1 with a PKC inhibitor experienced an initial increase in EPSP amplitude similar to that of preps exposed to NF1 alone, they experienced a subsequent drop in EPSP amplitude relative to baseline levels, indicating that PKC is involved in the effects of NF1 in that it plays a role in sustaining EPSP amplitude. Preps exposed to NF1 and a general protein kinase inhibitor experienced a greater drop in EPSP amplitude than those exposed to NF1 and a PKC inhibitor, indicating that PKC is not the only protein kinase involved in the effects of NF1, inviting further research into the roles of other protein kinases in NF1’s effects. Our research fills a gap in the current literature, as although previous studies indicated the role of PKC in the effects of DF2, a similar FMRFamide, we did not find any existing literature on the role of PKC in the effects of NF1.