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Dopamine Presynaptically Depresses Fast Inhibitory Synaptic Transmission via D4 Receptor-Protein Kinase A Pathway in the Rat Dorsolateral Septal Nucleus

¹Departments of Physiology and ²Neuropsychiatry, Kurume University School of Medicine, and ³Cognitive and Molecular Research Institute of Brain Diseases, Open Research Center, Kurume University, Kurume, Japan

Submitted 14 September 2005; accepted in final form 19 April 2006

The lateral septal nucleus receives a diffuse dopaminergic input originating from the ventral tegmental area of the brain stem. We examined whether dopamine (DA) modulates synaptic transmission in the slice preparation of the rat dorsolateral septal nucleus (DLSN). Bath application (10–15 min) of DA (30 µM) markedly depressed the amplitude of fast and slow inhibitory postsynaptic potentials (IPSPs) in DLSN neurons, while it produced only a minor depression of the amplitude of excitatory postsynaptic potentials (EPSPs) obtained in the presence of bicuculline. DA (30 µM) depressed the monosynaptic fast IPSP to 50% of control, but did not depress the inward current (I_GABA) induced by exogenous -aminobutyric acid (GABA). DA decreased the frequency of miniature fast IPSPs (m-fIPSPs) without significantly changing their amplitude. PD 168077, a selective D4 receptor agonist, depressed the fast and slow IPSPs but not the EPSP and decreased the frequency of m-fIPSPs. Both DA and PD 168077 increased the paired-pulse ratio of the monosynaptic fast IPSP. The inhibitory effect of DA on the fast IPSP was significantly attenuated by L-741,742, an antagonist at D4 receptors, but not by SCH 23390 and sulpiride, a D1-like and a D2-like receptor antagonist, respectively. N-ethylmaleimide, a blocker of pertussis toxin (PTX)-sensitive G protein (G_i/o), attenuated the DA-induced depression of the fast IPSP. N-[2-((p-bromocinnamyl) amino)ethyl]-5-isoquinoline sulfonamide, a protein kinase A (PKA) inhibitor, attenuated the DA-induced depression of the fast IPSP. These results suggest that DA inhibits spontaneous and evoked release of GABA via the D4 receptor-G_i-protein-PKA system in DLSN neurons.

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