Journal: Molecular Pain

Article Title: Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia

doi: 10.1186/1744-8069-3-17

Figure Lengend Snippet: NKCC1 inhibitor bumetanide blocks intracolonic capsaicin-evoked referred allodynia and hyperalgesia . Three doses of bumetanide or vehicle (VEH) were injected intrathecally (IT) and saline or capsaicin was injected into the colon 5 min later. A and B) Baseline response frequencies to abdominal 1 mN and 32 mN von Frey hair application are shown as well as 30 min after the intracolonic (IC) saline injection. C and D) Response frequencies to abdominal 1 mN (C) and 32 mN (D) von Frey hair application 30 min after the IC capsaicin injection are shown in comparison to baseline von Frey response frequencies. Stars (*) indicate significant effects vs. baseline (two-way anova); number signs (#) indicate significant effects of IT bumetanide injections (one-way anova, # or * p < 0.05, ** p < 0.01, *** p < 0.001; n = 6 per group).

Article Snippet: Bumetanide (BUM; Sigma, St. Louis, MO), AMG 9810 (Tocris) and n-arachidonoyl- dopamine (NADA, Tocris) were dissolved in artificial cerebrospinal fluid (aCSF) vehicle.

Techniques: Injection

Journal: Molecular Pain

Article Title: Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia

doi: 10.1186/1744-8069-3-17

Figure Lengend Snippet: Time course of NKCC1 inhibitor bumetanide blockade of intracolonic capsaicin-evoked referred allodynia . Bumetanide (BUM) or vehicle (VEH) was injected intrathecally (IT) 5 min prior to intracolonic (IC) capsaicin (A) or 20 min (B) or 4 hrs (C) after IC capsaicin. Response frequencies to 1 mN von Frey hair application to the abdomen are shown at the indicated time points post IC capsaicin. Stars (*) indicate significant effects of BUM vs. VEH (two-way anova) while number signs (#) indicate significant effects vs. baseline (BL) at a given time point (one-way anova, # or * p < 0.05, ## or ** p < 0.01, ### or *** p < 0.001; n = 6 per group).

Article Snippet: Bumetanide (BUM; Sigma, St. Louis, MO), AMG 9810 (Tocris) and n-arachidonoyl- dopamine (NADA, Tocris) were dissolved in artificial cerebrospinal fluid (aCSF) vehicle.

Techniques: Injection

Journal: Molecular Pain

Article Title: Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia

doi: 10.1186/1744-8069-3-17

Figure Lengend Snippet: NADA-evoked stroking allodynia is TRPV1-dependent and inhibited by bumetanide . The endogenous TRPV1 agonist NADA (10 nmol) or vehicle (VEH) was injected intrathecally (IT) with or without a co-injection of the TRPV1 antagonist AMG 9810 (1 nmol) and the hindpaws were stimulated with a cotton bud 15 (A) and 60 min (B) after the IT injection. NADA (10 nmol) or VEH was injected IT with or without a co-injection of the NKCC1 antagonist bumetanide (BUM, 1 nmol) and the hindpaws were stimulated with a cotton bud 15 (C) and 60 min (D) after the IT injection. Response frequencies to the cotton bud stimulation are shown. Stars (*) above columns indicate significant effects of NADA vs. VEH while number signs (#) above horizontal bars indicate significant effects of antagonists (one-way anova, * or # p < 0.05, ** or ## p < 0.01; n = 6 per group).

Article Snippet: Bumetanide (BUM; Sigma, St. Louis, MO), AMG 9810 (Tocris) and n-arachidonoyl- dopamine (NADA, Tocris) were dissolved in artificial cerebrospinal fluid (aCSF) vehicle.

Techniques: Injection