AIM: To investigate the effect of nicotine on β_1-adrenergic receptor (β_1-AR) in the hippocampal slice of rat. METHODS: Hippocampal slices (400 μm thick) were incubated in artificial cerebrospinal fluid (ACSF) previously saturated with 95％ O_2 and 5％ CO_2 at 28℃ for 120 min, and then incubated with nicotine 10 μmol/L for 30, 60, 90, and 120 min. mRNA of the β_1-adrenergic receptor was examined with semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), and the protein level was measured by Western blot and RIA. RESULTS: The mRNA gene expression and the protein level of β_1-adrenergic receptor in hippocampal slices were increased after nicotine treatment. The peak of protein occurred later but higher than that of mRNA level. CONCLUSION: Both expression of β_1-adrenergic receptor gene transcription and post-transcriptional protein level in rat hippocampus were altered by nicotine. AIM: To investigate the effect of nicotine on β_1-adrenergic receptor (β_1-AR) in the hippocampal slice of rat. METHODS: Hippocampal slices (400 μm thick) were incubated in artificial cerebrospinal fluid (ACSF) previously saturated with 95% 5% CO 2 at 28 ℃ for 120 min and then incubated with nicotine 10 μmol / L for 30, 60, 90 and 120 min. MRNA of the β 1-adrenergic receptor was examined with semiquantitative reverse transcription-polymerase chain reaction (RT- PCR), and the protein level was measured by Western blot and RIA. RESULTS: The mRNA gene expression and the protein level of β_1-adrenergic receptor in hippocampal slices were increased after nicotine treatment. The peak of protein occurred later but higher than that of mRNA level. CONCLUSION: Both expression of β_1-adrenergic receptor gene transcription and post-transcriptional protein level in rat hippocampus were altered by nicotine.