Pertussis toxin-sensitive G proteins mediate the inhibition of basal phosphoinositide metabolism caused by adenosine A1 receptors in rat hippocampal slices

The adenosine A(1) receptor selective agonist, N-6-cyclopentyladenosine (CPA, 300 nM) inhibited basal accumulation of [H-3]inositol phosphates ([H-3]InsPs), but not the total levels of membrane [H-3]-phosphoinositides, in rat hippocampal slices. This action of CPA was not significantly modified when synaptic transmission was blocked with tetrodotoxin (TTX, 200 nM) but was prevented in slices pre-incubated with pertussis toxin (PTX, 5 mug/mL) for 12-16 hr. Neither PTX nor TTX, when applied in the absence of CPA, influenced basal [H-3]InsPs accumulation. It is concluded that the inhibition of the basal phosphatidylinositol metabolism by adenosine A(1) receptor activation is independent of neurotransmission and involves a PTX-sensitive G protein, probably of the G(i)/G(o) family.