Ventral pallidal neuronal responses to dopamine receptor stimulation in the nucleus accumbens.

The possible role of ventral pallidum (VP) in expressing dopaminergic actions in the nucleus accumbens was studied electrophysiologically using extracellular single unit recording and iontophoretic techniques in urethane-anaesthetized rats. Microinjections of dopamine (130 mM, 5-10 micrograms/0.2-0.4 microliters) into the nucleus accumbens resulted in a gradual, but prolonged, increase in the firing rate of VP neurones. Injections of the D1 agonist SKF38393 (34 mM, 2 micrograms/0.2 microliters), followed by the D2 agonist quinpirole (40 mM, 2 micrograms/0.2 microliters) into the accumbens, but not in the reverse order, resulted in a similar increase in the activity of VP neurones, mimicking the dopaminergic effect. Injections of either the D1 or the D2 agonist alone into the accumbens, however, produced no significant changes. Furthermore, iontophoretic application of picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, or naloxone, an opiate (including enkephalin) antagonist on the same VP neurone which responded to accumbens dopamine injection also increase its spontaneous firing rate. Thus, pre-activation of D1 receptors in the accumbens was essential for the subsequent physiological expression of D2 receptors in inducing an increase in the firing rate of VP neurones. Dopamine in the accumbens may suppress the tonic inhibitory GABAergic and enkephalinergic outputs to the VP, resulting in an increase in firing rate of VP neurones. Since previous behavioural studies have shown that dopaminergic stimulation in the accumbens increases locomotor activity, the increased firing rate of ventral pallidal neurones may be expressing the postsynaptic actions of dopamine receptor stimulations in the accumbens as initiation of locomotor activity.