Abstract
The disorder of dopamine (DA) system may be related to neurodevelopmental dysfunction. However, the action of DA on synaptic transmission during development is largely unknown. We studied the effect of DA on GABAergic and glutamatergic transmission in neonatal rat hippocampus from the early period of synapse formation by whole-cell patch-clamp recordings from CA1 pyramidal cells. DA (100 μM) profoundly decreased the amplitude of GABAA receptor-mediated postsynaptic currents (GABAA-PSCs) to 32% in the first postnatal week, when GABA provides excitatory drive. DA also decreased the amplitude of AMPA receptor-mediated excitatory postsynaptic currents (EPSCs) to 29% in the second postnatal week, when glutamate responses first appear. The DA-induced inhibition declined after these periods and became only partial after postnatal day 30. Further we identified the receptor subtype involved in the DA-induced inhibition as phosphatidylinositol (PI)-linked D1-like receptor, since SKF 83959, a selective agonist for PI-linked D1-like receptor, clearly mimicked the action of DA, and U-73122, an inhibitor of phospholipase C, significantly reduced the DA-induced inhibition. DA did not change the response to puff-applied GABA or kainic acid, nor miniature GABAA-PSC or EPSC amplitudes. These results suggest that the activation of PI-linked D1-like receptor profoundly suppresses the excitatory transmission in the developing hippocampus by presynaptic mechanisms. [J Physiol Sci. 2006;56 Suppl:S160]
