PKC mediated interaction between arachidonic acid and metabotropic glutamate receptors potentiates synaptic transmission in the rat hippocampal slice

Perfusion of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 50 mu M) caused a transient depression of the field excitatory postsynaptic potential (fEPSP) recorded from the CA1 region of the rat hippocampal slice. Perfusion of arachidonic acid (10 mu M) alone had no effect on synaptic transmission, however, coperfusion of ACPD and arachidonic acid caused a slowly rising and persistent potentiation of the fEPSP. This effect was blocked by the selective protein kinase C (PKC) inhibitors hypericin (40 mu M) and chelerythrine (5 mu M). Neither methyl-arachidonic acid (10 mu M), nor oleic acid (10 mu M), mimicked arachidonic acid in producing the persistent potentiation. The results suggest that arachidonic acid and ACPD interact to modulate synaptic transmission by a process which relies on a synergistic, but indirect, activation of PKC.