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Koh, Wei Choon Alvin,Chandra, Pranjal,Kim, Dong-Min,Shim, Yoon-Bo American Chemical Society 2011 ANALYTICAL CHEMISTRY - Vol.83 No.16
<P>Novel nanostructures of gold nanoparticle (AuNP) encapsulated-conductive polymer have been developed to study biosensor probe materials and utilized to detect the concentration of inducible nitric oxide synthase (iNOS). A 2,2′:5′,5″-terthiophene-3′-benzoic acid (TTBA) monomer was synthesized and self-assembled on gold nanoparticles (AuNPs). The size effects of the AuNPs and TTBA monomer film thickness on the electrode conductivity were examined. Anti-iNOS antibody was covalently bound on an encapsulated-AuNPs polymer layer with self-assembled TTBA. The immunocomplex formation between iNOS and anti-iNOS was directly observed by cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS). This study looked at the applicability of the self-assembled TTBA layer where the results indicated an efficient electrochemical response toward iNOS. The calibration plot of the current response vs. iNOS concentration exhibited a linear relationship in the range of 0.001–0.02 μg/mL. The calibration sensitivity of iNOS was 59.4 ± 0.3 mV/μg mL<SUP>–1</SUP>. The detection limit of iNOS was determined to be 0.20 ± 0.04 ng/mL based on five time measurements (95% confidence level, <I>k</I> = 3, <I>n</I> = 5). Further results show that AuNP-encapsulated conductive polymers are good nanostructured materials as biosensor probes and have a potential application in cell biosensors.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/ancham/2011/ancham.2011.83.issue-16/ac2006558/production/images/medium/ac-2011-006558_0004.gif'></P>
이동근,최은상,안성민,심윤보,Wei Choon Alvin Koh,심인섭 한국뇌신경과학회 2011 Experimental Neurobiology Vol.20 No.2
Alterations in nitric oxide (NO) release in response to psychostimulants in the striatum cause a plastic change contributing to the development and expression of addiction. In this study, regulation of NO efflux evoked by acute cocaine in the dorsal striatum was investigated using real-time detection of NO in vivo. We found that acute systemic injection of cocaine (20 mg/kg) increased NO efflux, which was reduced by the intrastriatal infusion of the dopamine D1 receptor antagonist, SCH23390 (7.5 nmol), and the dopamine D2 receptor agonist, quinpirole (5 nmol). Increased levels of NO efflux by acute cocaine were also reduced by the intrastriatal infusion of the N-methyl-D-aspartate (NMDA) receptor antagonists, MK801 (2 nmol) and AP5 (2 nmol). These findings suggest that interactions of dopamine D1 receptors and NMDA receptors after acute exposure to cocaine participate in the upregulation of NO efflux in the dorsal striatum.