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. 2016 Aug 31;4:92. doi: 10.3389/fcell.2016.00092

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.”