Promotion of HFS-induced LTP at the SC-CA1 synapses by 14,15-EET and TPPU was blocked by an NR2B antagonist.
Thus, cAMP-PDE-adenosine signaling is involved in TPPU and 14,15-EET modulation of presynaptic glutamate release and plasticity at the hippocampal synapses [50, 51].
Additionally, we showed that TPPU and 14,15-EET promoted FSK-mediated LTP and increased the phosphorylation of GluR1.
We demonstrated that TPPU and 14,15-EET induced increased phosphorylation of CaMKII at Thr-286, phosphorylation of NR2B at Tyr-1472, and phosphorylation of GluR1 at Ser-831 to strengthen the glutamate-mediated synaptic plasticity.
Caption: Figure 1: Acute TPPU and 14,15-EET applications increased excitatory synaptic transmission at the Schaffer collateral-CA1 hippocampal synapses.
(a) Effects of TPPU (0.1 [micro]M) and 14,15-EET (30 nM) on the enhancement of HFS-induced LTP.
Caption: Figure 3: TPPU and 14,15-EET facilitated FSK-induced LTP.
(a) Effects of TPPU and 14,15-EET on forskolin-induced LTP in the presence of Ro 20-1724 (10 [micro]M).
Caption: Figure 5: Phosphorylation of glutamate receptors in the hippocampus was increased by TPPU and 14,15-EET.