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Volume 16, Number 23, Issue of December 1, 1996 pp. 7505-7512
Copyright ©1996 Society for Neuroscience

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

Received July 8, 1996; revised Sept. 10, 1996; accepted Sept. 16, 1996.

Toshihiko Momiyama¹ and J. A. Sim²

¹ Department of Pharmacology, University College London, London WC1E 6BT, United Kingdom, and ² Department of Neurobiology, Babraham Institute, Cambs CB2 4AT, United Kingdom

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 (K_B 0.82 µM), whereas S()-eticlopride, a D₂-like antagonist, showed slight antagonism (K_B 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.

Key words: dopamine; D₁ receptor; inhibitory postsynaptic currents; magnocellular basal forebrain nuclei; presynaptic modulation

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