Modulation by desensitized nicotinic receptors on metabolism of DA in striatum derived from the hemiparkinsonian model

Streptococcus mutans is a common Gram-positive bacterium and plays a significant role in dental caries. Tobacco and/or nicotine have documented effects on S. mutans growth and colonization. Sortase A is used by many Gram-positive bacteria, including S. mutans, to facilitate the insertion of certain cell surface proteins, containing an LPXTGX motif such as antigen I/II. This study examined the effect of nicotine on the function of sortase A to control the physiology and growth of S. mutans using wild-type S. mutans NG8, and its isogenic sortase-defective and-complemented strains. Briefly, the strains were treated with increasing amounts of nicotine in planktonic growth, biofilm metabolism, and sucrose-induced and saliva-induced antigen I/II-dependent biofilm formation assays. The strains exhibited no significant differences with different concentrations of nicotine in planktonic growth assays. However, they had significantly increased (Pf0.05) biofilm metabolic activity (2-to 3-fold increase) as the concentration of nicotine increased. Furthermore, the sortase-defective strain was more sensitive metabolically to nicotine than the wild-type or sortase-complemented strains. All strains had significantly increased sucrose-induced biofilm formation (2-to 3-fold increase) as a result of increasing concentrations of nicotine. However, the sortase-defective strain was not able to make as much sucrose-and saliva-induced biofilm as the wild-type NG8 did with increasing nicotine concentrations. These results indicated that nicotine increased metabolic activity and sucrose-induced biofilm formation. The saliva-induced biofilm formation assay and qPCR data suggested that antigen I/II was upregulated with nicotine but biofilm was not able to be formed as much as wild-type NG8 without functional sortase A.

烟碱上调大鼠海马脑片b1-肾上腺素能受体基因转录

AIM: To investigate the effect of nicotine on 1β1-adrenergic receptor (β1-AR) in the hippocampal slice of rat. METHODS: Hippocampal slices (400 μm thick) were incubated in artificial cerebrospinal fluid (ACSF) previously saturated with 95 % O2 and 5 % CO2 at 28 ℃ for 120 min, and then incubated with nicotine 10 μmol/L for 30, 60, 90, and 120 min. mRNA of the β1-adrenergic receptor was examined with semiquantitative reverse transcriptionpolymerase 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 β1-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 β1- adrenergic receptor gene transcription and post-transcriptional protein level in rat hippocam pus were altered by nicotine.