Abstract
We examined the effects of dopamine (DA) on the excitatory postsynaptic potential (EPSP) in neurons of the rat dorsolateral septal nucleus (DLSN) by conventional intracellular recording and voltage-clamp methods. A continuous application of DA (1 μM, for 30-60 min) produced a gradual increment of the amplitude of the EPSPs (149 ± 19% of control, n=8). The long-lasting enhancement of the EPSP was mimicked by SKF 38393 (10 μM), a D1 type receptor agonist, but not by quinpirole (10 μM) and PD 168077 (3 μM), D2 type and D4 receptor antagonists, respectively. The SKF 38393-induced enhancement of the EPSP was blocked by SCH 23390 (10 μM), a D1 type receptor antagonist, but not by sulpiride (5 μM) and L-741742 (10 μM), antagonists for D2 type and D4 type receptors, respectively. SKF 38393 increased the amplitude of miniature EPSPs without changing their frequencies. SKF 38393 enhanced the exogenous glutamate-induced responses in DLSN neurons. The ratio of the paired-pulse facilitation of the EPSP was not altered by SKF 38393. Application of dibutyryl cyclic AMP (1 mM) or forskolin (10 μM) mimicked the effect of DA on the EPSP. The SKF 38393-induced enhancement of the EPSP was blocked by H-89 (10 μM), an inhibitor for protein kinase A (PKA) but not by calphostin C (100 nM), an inhibitor for PKC. These results suggest that DA enhances the EPSP by increasing evoked release of glutamate via the postsynaptic D1 receptors-PKA pathway in rat DLSN neurons. [J Physiol Sci. 2007;57 Suppl:S146]
