Protein Kinase C is Partially responsible for the Effects of NF1 in Sustaining EPSP Amplitude Increase

Abstract

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.