Dopamine depresses glutamatergic synaptic transmission in the rat parabrachial nucleus in vitro

Nyslatin-perforated patch recordings were made from rat parabrachial neuron s in an in vitro slice preparation to examine the effect of dopamine on par abrachial cells and on excitatory synaptic transmission in this nucleus. In current clamp mode, dopamine reduced the amplitude of the evoked excitator y postsynaptic potential without significant change in membrane potential. In cells voltage-clamped at -65 mV, dopamine dose dependently and reversibl y decreased evoked, pharmacologically isolated, excitatory postsynaptic cur rents with an EC50 of 31 mu M. The reduction in excitatory postsynaptic cur rent was accompanied by an increase in paired purse ratio (a protocol used to detect presynaptic site of action) with no change in the holding current or in the decay of the evoked excitatory postsynaptic currents. In additio n, dopamine altered neither postsynaptic(+/-)-alpha-amino-3-hydroxy-5-methy lisoxazole-4-propionate-induced currents, nor steady-slate current voltage curves. Miniature excitatory postsynaptic current analysis revealed that do pamine caused a rightward shift of the frequency-distribution curve with no change in the amplitude-distribution curve, which is consistent with a pre synaptic mechanism. The dopamine-induced attenuation of the excitatory post synaptic current was almost completely blocked by the D-1-like receptor ant agonist SCH23390 (10 mu M), although the D-2-like antagonist sulpiride (10 mu M) also partially blocked it. Combined application of both antagonists b locked all dopamine-induced synaptic effects. The synaptic effect of dopami ne was mimicked by the D-1-like agonist SKF38393 (50 mu M), but the D-2-lik e agonist quinpirole (50 mu M) also had a small effect. Combined applicatio n of both agonists did not produce potentiated responses. Dopamine's effect on the excitatory postsynaptic current was independent of serotonin, GABA and adenosine receptors, but may have some interactions with adrenergic rec eptors. These results suggest that dopamine directly modulates excitatory s ynaptic events in the parabrachial nucleus predominantly via presynaptic D- 1-like receptors. (C) 1999 IBRO. Published by Elsevier Science Ltd.