Fig. 2: Ketamine inhibition of BSM contraction is not mediated by NMDAR.
From: Disruption of Cav1.2-mediated signaling is a pathway for ketamine-induced pathology
Representative filters show UV light-illuminated urine spots from a wild type mouse (a n = 21 filters) and a smooth muscle-specific NR1 knockout (SMNR1KO) mouse (b n = 18 filters). Summarized quantitative data (c) indicate normal voiding volume, normal spot number per void, and normal spot size for SMNR1KO mice. ± in c is SD of the mean. In b 400 mm2 white box at bottom right serves as area standard. d–g BSM contraction in SMNR1KO mice stimulated by EFS (d wild type n = 8 BSM strips, SMNR1KO n = 8 BSM strips), by 10 µM carbachol (e wild type n = 8 BSM strips, SMNR1KO n = 8 BSM strips), by 10 µM α,β-meATP (f wild type n = 8 BSM strips, SMNR1KO n = 8 BSM strips), or by 50 mM KCl (g wild type n = 8 BSM strips, SMNR1KO n = 8 BSM strips). Data are shown as box and whiskers, center line is the median of the data set, box represents 75% of the data, and bars indicates whiskers from minimum to maximum. Data were analysed by Student’s t-test. h ketamine concentration-dependent inhibition of contraction of BSM from SMNR1KO mice (n = 12 BSM strips). The data indicate that NMDAR does not mediate ketamine-induced inhibition of BSM contraction. Data are presented as mean values ± SD. Source data are provided as a Source Data file.
