抄録
The abnormality of neonatal hippocampus may lead to the impairment of prefrontal cortex as observed in schizophrenia. Dopamine is related to such disorder. Recently the dysfunction of GABAergic interneurons has been suggested as the pathophysiology of schizophrenia. We have reported that dopamine profoundly suppresses GABAergic transmission in the neonatal rat hippocampus by a presynaptic manner (Noriyama et al., 2006). However, the effect of dopamine on spontaneous activities of GABAergic interneurons in the neonatal hippocampus is unknown. In this study, we studied the effect of dopamine on GABAergic interneurons in the neonatal mouse hippocampus by whole-cell patch clamp recordings from CA1 pyramidal cells. The amplitude of evoked GABAA-PSCs was decreased by dopamine. In contrast to the inhibitory effect on evoked GABAA-PSCs, the frequency and amplitude of spontaneous GABAA-PSCs were increased by dopamine in the neonatal mice. The effect on the frequency was reduced by D1 antagonists. Dopamine had no effect on minuature GABAA-PSCs. These results suggest that dopamine may increase the excitability of GABAergic interneurons. These complex effects of dopamine on GABAergic transmission may be related to the pathophysiology of schizophrenia. [J Physiol Sci. 2008;58 Suppl:S128]
