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The effects of dopamine (DA) on inhibitory transmission onto identified magnocellular neurons were examined in rat basal forebrain slices using whole-cell recording. IPSCs evoked by focal stimulation within basal forebrain nuclei were reversibly blocked by 10 μm bicuculline and had a decay time constant of 20.1 ± 0.77 msec in the presence of 6-cyano-7-nitroquinoxalline-2,3-dione (5 μm). Bath application of DA reduced the amplitude of IPSCs up to 71.1 ± 1.49% in a concentration-dependent manner between 0.003 and 1 mm (the IC50 value being 6.6 μm), without any effect on the holding current at −70 mV. DA (10 μm) reduced the frequency of miniature IPSCs (mIPSCs) recorded in the presence of TTX (0.5 μm), without affecting their mean amplitude, rise time, and decay time constant. Furthermore, the DA-induced effect on mIPSCs remained unaffected by 100 μm cadmium, suggesting a presynaptic mechanism independent of calcium influx. SKF 81297, a D1-like agonist, mimicked DA-induced effect on evoked IPSCs (IC50, 10.9 μm), whereas R(−)-TNPA or (−)-quinpirole, D2-like agonists (30 μm), had little or no effect on the amplitude of evoked IPSCs. R(+)-SCH 23390, a D1-like antagonist, antagonized the DA-induced effect on IPSCs (KB 0.82 μm), whereas S(−)-eticlopride, a D2-like antagonist, showed slight antagonism (KB 7.8 μm). Forskolin (10 μm) reduced the amplitude of evoked IPSCs to ∼58% of the control and occluded the inhibitory effect of DA. These findings indicate that DA reduces inhibitory transmission onto magnocellular basal forebrain neurons by activating presynaptic D1-like receptors.

Modulation of Inhibitory Transmission by Dopamine in Rat Basal Forebrain Nuclei: Activation of Presynaptic D1-like Dopaminergic Receptors

Modulation of Inhibitory Transmission by Dopamine in Rat Basal Forebrain Nuclei: Activation of Presynaptic D₁-like Dopaminergic Receptors