Table 1.
Involvement of DGK isoforms in several forms of synaptic plasticity.
| DGK isoform | Synapse | Localization | Tested forms of synaptic plasticity | Reported effects in KO mice | Known/expected functions of DGKs |
|---|---|---|---|---|---|
| DGKε | Perforant path-dentate granule cell synapses | N.D. | LTP | Reduction | Regulating amounts of DAG and PKC activity required for LTP, and regulating the lipid signaling leading to the production of retrograde messengers required for LTP |
| DGKζ | Hippocampal SC-CA1 synapses | Postsynaptic density | Postsynaptic LTP | Enhancement | Regulating amounts of DAG produced by mGluR activation, and balancing PKC activity, which is a modulator of LTP and LTD |
| Postsynaptic LTD | Reduction | ||||
| DGKβ | Hippocampal SC-CA1 synapses | Membranes including synaptic areas | Postsynaptic LTP | Reduction | Regulating basal DAG levels |
| DGKι | Hippocampal SC-CA1 synapses | Presynaptic areas | Presynaptic LTD | Reduction | Reducing DAG levels and consequently preventing the activation of target molecules that antagonize LTD |
| DGKκ | Hippocampal SC-CA1 synapses | N.D. | Postsynaptic LTP | Reduction | Regulating basal DAG levels |
| Postsynaptic LTD | Enhancement | ||||
| DGKζ | Cerebellar parallel fiber-Purkinje cell synapses | Postsynaptic areas | Postsynaptic LTP | Normal | – |
| Postsynaptic LTD | Reduction | Targeting PKCα required for LTD at synapses, maintaining optimal PKCα activity levels via reducing basal DAG levels, and receiving inhibition from PKCα |
N.D. stands for “not described or undetermined.”