抄録
Neurodevelopmental abnormalities in the medial temporal lobe including hippocampas are implicated in the pathophysiology of schizophrenia. The dysfunction of the dopaminergic system is of particular interest in schizophrenia. Dopamine can enhance or inhibit synaptic transmission in various brain regions. In the hippocampus of early neonatal rat, however, the modulatory effects of dopamine on synaptic transmission has not yet been clarified. In this study we studied the effect of dopamine on glutamatergic and GABAergic transmission during the period of synaptogenesis in rat hippocampus. Whole-cell patch clamp recordings were obtained from CA1 pyramidal cells. Dopamine (100μM) reversively attenuated the amplitude of excitatory postsynaptic currents (EPSCs) to 31.6 ± 7.3% of the control and the amplitude of GABAA receptor-mediated postsynaptic currents (GABAA-PSCs) to 32.2 ± 5.4% of the control. SKF38393, an agonist of D1-like receptors, decreased the amplitude of EPSCs and GABAA-PSCs, while the effect of dopamine was partially antagonized by SCH23390, an antagonist of D1-like receptors. Kainic acid (100μM)- or GABA (100μM)-induced inward currents were not changed by dopamine. Dopamine had no effect on the amplitude of miniature EPSCs or miniature GABAA-PSCs. In conclusion, dopamine depresses glutamatergic and GABAergic transmission in the hippocampus at the stage of synaptogenesis and the depression is thought to be mediated through D1-like receptors by presynaptic mechanism. [Jpn J Physiol 54 Suppl:S151 (2004)]
