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

The adenosine A1 receptor selective agonist, N6-cyclopentyladenosine (CPA, 300 nM) inhibited basal accumulation of [3H]inositol phosphates ([3H]InsPs), but not the total levels of membrane [3H]-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 microg/mL) for 12-16 hr. Neither PTX nor TTX, when applied in the absence of CPA, influenced basal [3H]InsPs accumulation. It is concluded that the inhibition of the basal phosphatidylinositol metabolism by adenosine A1 receptor activation is independent of neurotransmission and involves a PTX-sensitive G protein, probably of the Gi/Go family.