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. 2007 Dec 6;586(Pt 3):751–762. doi: 10.1113/jphysiol.2007.136440

Figure 5. Modulation of 5-HT3A receptor–channel properties by LC1 antisense oligonucleotides.

Figure 5

A, schematic illustration of the genomic structure of MAP1B-LC1. Note that the LC1 antisense oligo (ATS) is designed to target a segment crossing an axon (10)–intron border. B, RT-PCR of endogenous LC1 in HEK 293 cells after LC1-ATS and inverted control treatment. C, quantization of MAP1B mRNA by real-time PCR in HEK 293 cells after LC1-ATS treatment. The relative expression ratios of MAP1B mRNA were calculated by the formula: 2ΔCt, where ΔCt stands for the Ct (PCR cycle number when the signal reached the threshold) difference between groups. The filled bar represents average percentage expression of control (open bar, LC1-ATS untreated group). D, the effect of LC1-ATS on 5-HT3A receptor activation by LC1-ATS. Trace records of the current activated by 30 μm 5-HT are normalized. Bar graph represents average activation kinetics for 5-HT. E, modulation of 5-HT3A receptor desensitization by LC1-ATS. Trace records show decay of current in the presence of 30 μm 5-HT without (Ctr) and with pretreatment with LC1-ATS and inverted control. Bar graph represents average desensitization kinetics for 5-HT. Asterisk indicates a significant difference from control (unpaired t test, P < 0.01).