1. Experimental ulcers alter voltage-sensitive sodium currents in rat gastric sensory neurons 
K. Bielefeldt, N. Ozaki, G.F. Gebhart 
Gastroenterology 
Volume 122, Issue 2, Pages (February 2002)
DOI: /gast
Copyright © 2002 American Gastroenterological Association Terms and Conditions

2. Fig. 1
Voltage-sensitive sodium currents recorded from gastric sensory neurons. Representative current tracings obtained from (A and B) nodose and (C and D) DRG neurons by depolarizations from −70 mV to various test potentials between −60 mV and 40 mV are superimposed. The upper panel shows (A and C) TTX-sensitive; the lower panel shows (B and D) TTX-resistant current.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

3. Fig. 2
Voltage-dependence of sodium currents recorded from gastric sensory neurons. The voltage dependence of activation and inactivation was determined for (A and B) nodose and (C and D) T9, T10 DRG neurons. Sodium currents were differentiated based on their pharmacologic properties as TTX-sensitive (open symbols) and TTX-resistant (closed symbols) currents. To determine the voltage dependence of activation, cells were stepped from −70 mV to various test potentials between −60 mV and 40 mV. The results were converted into normalized conductance {C = (I / Imax)/(V − Vreversal)} and fitted by the Boltzmann equation (broken lines) for (A) nodose and (C) DRG neurons. To determine the voltage-dependence of inactivation, cells were held at potentials between −110 mV and 20 mV for 750 ms before stepping to a test potential of 10 mV. The results were normalized and fitted by the Boltzmann equation (broken lines) for (B) nodose and (D) DRG neurons. See text for details.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

4. Fig. 3
Time course of recovery from inactivation. To determine the recovery from inactivation, cells were depolarized from −70 mV to 10 mV for 15 ms, followed by a second test pulse to 10 mV after repolarization to −70 mV for 2 to 200 ms. The upper panel shows superimposed sample traces obtained during the second test pulse from cells expressing (A) TTX-sensitive and (B) TTX-resistant sodium current (calibration bars 1 nA and 5 ms, respectively). The time course of recovery is summarized in the lower panel for TTX-sensitive (open symbols) and TTX-resistant (closed symbols) currents. The experimental data were fitted to a single exponential (broken lines) for (C) nodose and (D) DRG neurons.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

5. Fig. 4
Histologic changes after submucosal injection of HAc or saline. (A) Microscopic confirmation of an ulcer in the glandular stomach induced by HAc-injection. (B) Representative section of the glandular stomach in ulcer-free areas after HAc-injection showing thickening of the gastric wall, inflammatory infiltrate in submucosa and muscularis, and partial necrosis of the muscularis. In contrast, (C) saline injection did not lead to significant inflammation.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

6. Fig. 5
Effect of gastric inflammation on the voltage-dependence of sodium currents in nodose neurons. The voltage dependence of activation and inactivation were determined for neurons obtained from saline (closed symbols) and HAc-treated animals (open symbols) as described in Figure 2. The results for the TTX-sensitive and TTX-resistant panel are summarized in panels A and B, and C and D, respectively. See text for details.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

7. Fig. 6
Effect of gastric inflammation on the time course of recovery from inactivation of nodose neurons. To determine the recovery from inactivation, cells were depolarized from −70 mV to 10 mV for 15 ms, followed by a second test pulse to 10 mV after repolarization to −70 mV for 2 to 200 ms. The peak current recorded during the second test pulse was normalized and plotted as (A) a function of time for control conditions (closed symbols; n = 61) and cells obtained from HAc-treated animals (n = 43; open symbols). The results were fitted by a double exponential (broken line). The recovery kinetics were analyzed for (B) the TTX-sensitive and (C) the TTX-resistant current currents and fitted with a single exponential.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

8. Fig. 7
Effect of gastric inflammation on the voltage-dependence of sodium currents in T9, T10 DRG neurons. The voltage dependence of activation and inactivation were determined for neurons obtained from saline (closed symbols) and HAc-treated animals (open symbols) as described in Figure 2. The results for the TTX-sensitive and TTX-resistant panel are summarized in panels A and B, and C and D, respectively. See text for details.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions

9. Fig. 8
Effect of gastric inflammation on the time course of recovery from inactivation of in T9, T10 DRG neurons. To determine the recovery from inactivation, cells were depolarized from −70 mV to 10 mV for 15 ms, followed by a second test pulse to 10 mV after repolarization to −70 mV for 2 to 200 ms. The peak current recorded during the second test pulse was normalized and plotted as (A) a function of time for control conditions (closed symbols; n = 21) and cells obtained from HAc-treated animals (n = 18; open symbols). The results were fitted by a double exponential (broken line). The recovery kinetics were analyzed for the (B) TTX-sensitive and (C) the TTX-resistant currents and fitted with a single exponential.
Gastroenterology  , DOI: ( /gast )
Copyright © 2002 American Gastroenterological Association Terms and Conditions