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 α1-adrenoceptor agonists (phenylephrine or noradrenaline) or these α1-adrenoceptor agonists along with prazosin, an α1-adrenoceptor antagonist. In cortical synaptosomes both α1-adrenoceptor agonists increased the basal release of [3H]NA in a concentration-dependent manner (EC50 = 0.15 μM for phenylephrine and 12.6 μM for noradrenaline). Effects were reversed by 0.01 μM prazosin (EC50 = 2.46 and 130.1 μM, respectively). In synaptosomes from rat brain hippocampus, phenylephrine (EC50 = 1.28 μM) and noradrenaline (EC50 = 33.7 μM) also increased the [3H]NA release and prazosin (0.01 μM) shifted the corresponding concentration-response curves to the right (EC50 = 7.38 and 264.0 μM, respectively). Events produced by noradrenaline acting as α1-adrenoceptor agonist did not show Ca2+ dependence. These results suggest (1) the presence of functional α1-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 Ca2+ may be involved.
- 1 -Adrenoceptors
- [ H]Noradrenaline release 3