Abstract
We have investigated the type of purine receptor in the guinea-pig olfactory cortex, using pial surface slices maintained in vitro. Adenosine (0.1 to 100 μmol/l) bath applied in the presence of the uptake inhibitor nitrobenzylthioinosine, depressed the evoked potentials in a dose related fashion. Synthetic and uptake resistant adenosine analogues had the same effect as adenosine and the order of potency of these was: 5′-N-ethylcarboxamide adenosine> l-N6-phenylisopropyl adenosine (l-PIA)=N6-cyclohexyladenosine=2-chloroadenosine > adenosine > d-N6-phenylisopropyladenosine (d-PIA). Thed-stereoisomer of PIA was 45 times less potent thanl-PIA. The methylxanthine compounds 8-phenyltheophylline (3 μmol/l) and 3-isobutyl-1-methylxanthine (50 μmol/l) antagonised the depression produced byl-PIA. Rolipram, a phosphodiesterase inhibitor, in concentrations up to 100 μmol/l had no effect on the evoked potentials or on adenosine action. Forskolin, a cAMP stimulant, slightly increased the amplitude of the evoked potential, and partly reversed the depressant effect of adenosine. Noradrenaline had no effect either alone or in the presence of adenosine. The results of these experiments indicate the existence of A1 subtype adenosine receptors in the guinea pig olfactory cortex probably linked to a depression of intracellular cAMP.