The modulatory effects of noradrenergic agonists on the 25 mM K+-induced release of [3H]dopamine (3H-DA) from rat brain nucleus accumbens slices was investigated, using a superfusion technique. The K+-induced release of 3H-DA was Ca2+ dependent, significantly enhanced (25-32%; p less than 0.02) by the beta-adrenoceptor agonist isoproterenol (10 microM), and significantly decreased (13-25%; p less than 0.05) by the alpha 2-adrenoceptor agonist clonidine (10 microM). At these concentrations neither drug affected basal release of 3H-DA. Clonidine (100 microM) increased the basal release of 3H-DA, while decreasing the K+-induced release by 19% (p less than 0.01). The inclusion of desipramine in the incubation medium, to prevent accumulation of 3H-DA into noradrenergic neurons, did not alter the inhibitory effect of clonidine (10 microM) on 3H-DA release. This study provides direct evidence that noradrenergic neurons can modulate dopaminergic neurotransmission in the mesolimbic system.

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The effect of serotonin agonists on the depolarization (K+)-induced, calcium-dependent, release of [3H]dopamine (DA) from rat nucleus accumbens and striatal slices was investigated. Serotonin enhanced basal 3H overflow and reduced K+-induced release of [3H]DA from nucleus accumbens slices. The effect of serotonin on basal 3H overflow was not altered by the serotonin antagonist, methysergide, or the serotonin re-uptake blocker, chlorimipramine, but was reversed by the DA re-uptake carrier inhibitors nomifensine and benztropine. With the effect on basal overflow blocked, serotonin did not modulate K+-induced release of [3H]DA in the nucleus accumbens or striatum. The serotonin agonists, quipazine (in the presence of nomifensine) and 5-methoxytryptamine, did not significantly affect K+-induced release of [3H]DA in the nucleus accumbens. This study does not support suggestions that serotonin receptors inhibit the depolarization-induced release of dopamine in the nucleus accumbens or striatum of the rat brain. The present results do not preclude the possibility that serotonin may affect the mesolimbic reward system at a site which is post-synaptic to dopaminergic terminals in the nucleus accumbens.

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