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Fig. 1 | Molecular Brain

Fig. 1

From: Stress-induced antinociception to noxious heat requires α1A-adrenaline receptors of spinal inhibitory neurons in mice

Fig. 1

α1A-ARs in spinal inhibitory neurons contribute to acute restraint stress-induced antinociception to noxious heat. a, b Latency to evoke nociceptive behaviors (licking or jumping) by noxious heat stimulation (hot-plate test) following acute restraint stress for 2 h in Adra1aflox/flox mice (n = 9) and Vgat-Cre;Adra1aflox/flox mice (n = 8) (a), and WT mice pretreated intraperitoneally with saline (n = 10) or DSP-4 (n = 10) (b). **P < 0.01 and ****P < 0.0001 vs. Pre-stress, #P < 0.05 and ##P < 0.01 vs. saline-treated mice and Adra1aflox/flox mice at post-stress (0 min), respectively. c Frequency and amplitude of sIPSCs in SG neurons in spinal cord slices from Adra1aflox/flox mice or Vgat-Cre;Adra1aflox/flox mice before (Pre NA) and after NA (20 μM) application (Post NA) (n = 14–15 neurons). *P < 0.05, **P < 0.01, ##P < 0.01. d Effect of silodosin (Silo: 40 nM) on NA-induced facilitation of sIPSC frequency in SG neurons (n = 9–10 neurons). ****P < 0.0001. e Latency to evoke nociceptive behaviors (licking or jumping) in hot-plate test at 10 min after intrathecal administration of NA (10 nmol, n = 7) or phenylephrine (Phe: 50 nmol, n = 8) in Adra1aflox/flox mice or Vgat-Cre;Adra1aflox/flox mice, *P < 0.05, **P < 0.01, ##P < 0.01, and ###P < 0.001. Data show the mean ± SEM

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