Functional and Physical Interaction of Diacylglycerol Kinase ζ with Protein Kinase Cα Is Required for Cerebellar Long-Term Depression.

Many studies have identified signaling molecules that mediate long-term synaptic plasticity. In the basal state, the activities and concentrations of these signaling molecules must be maintained at low levels, yet be ready to be boosted, so that synapses can undergo synaptic plasticity only when they are stimulated. However, the mechanisms involved in creating such conditions are not well understood. Here, we show that diacylglycerol kinase ζ (DGKζ) creates optimal conditions for the induction of cerebellar long-term depression (LTD). DGKζ works by regulating localization and activity of protein kinase Cα (PKCα), an important mediator of LTD, so that PKCα effectively responds to the stimulation that triggers LTD.