Possible involvement of α 1-adrenoceptors in the modulation of [ 3H]noradrenaline release in rat brain cortical and hippocampal synaptosomes

Nerve terminals obtained from rat brain cortex and hippocampus, were labelled with 0.04 μM of [ 3H]noradrenaline ([ 3H]NA). Thereafter the basal release of [ 3H]NA was measured in a Brandel superfusion apparatus, in the presence of α 1-adrenoceptor agonists (phenylephrine or noradrenaline) or there α 1-adrenoceptor agonists along with prazosin, an α 1-adrenoceptor antagonists, In cortical synaptosomes both α 1-adrenoceptor agonists increased the basal release of [ 3H]NA in a concentration-dependent manner (EC 50=0.15 μM for phenylephrine and 12.6 μM for noradrenaline). Effects were reversed by 0.01 μM prazosin (EC 50 = 2.46 and 130.1 μM, respectively). In synaptosomes from rat brain hippocampus, phenylephrine (EC 50 = 1.28 μM) and noradrenaline (EC 50 = 33.7 μM) also increased the [ 3H]NA release and prazosin (0.01 μM) shifted the corresponding concentration-response curves to the right (EC 50 = 7.38 and 264.0 μM, respectively). Events produced by noradrenaline acting as α 1-adrenoceptor agonist did not show Ca 2+ dependence. These results suggest (1) the presence of functional α 1-adrenoceptors in nerve terminals from rat brain cortex and hippocampus, (2) that these receptors seem to play a role in the presynaptic modulation of [ 3H]NA release, and (3) that intraterminal Ca 2+ may be involved.