Membrane traffic is one of the important functions in a variety of animal cells, which includes vesicular transportation, secretion and morphologic transformation of organelles. To investigate roles of the membrane traffic on the neuronal functions, we analyzed pharmacological effects of Brefeldin-A, a drug which is known to disassemble Golgi apparatus, on synaptic responses in the CNS neurons. Hippocampal slices were prepared from 3-5 weeks old mice, and field EPSPs (fEPSPs) were recorded from stratum radiatum of the CA1 region. Brefeldin-A was solved into methanol, and then into normal ACSF at a final concentration (0.1-1μg/ml). The drug solution was continuously applied 10 min during a record session. Five to fifteen minutes after application, maximum slope of fEPSP transiently decreased to 50-70% and then increased to 150-200% of control. This augmentation maintained at least 2 hrs in all slices examined, and was inhibited in the presence of BAPTA-AM, an intracellular Ca²⁺ chelator. After drug application, paired-pulse facilitation ratio of the fEPSP was decreased because the slope of first fEPSP was increased although the second one did not increase. These results suggest that Brefeldin-A enhance excitatory synaptic transmission in the hippocampal CA1 region. An increase in intracellular Ca²⁺ at pre- and/or postsynaptic sites is assumed to be a factor in the induction of potentiation. [Jpn J Physiol 55 Suppl:S150 (2005)]