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"Intensity-response" effects of electroacupuncture on gastric motility and its underlying peripheral neural mechanism.

Su YS, He W, Wang C, Shi H, Zhao YF, Xin JJ, Wang XY, Shang HY, Hu L, Jing XH, Zhu B - Evid Based Complement Alternat Med (2013)

Bottom Line: The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA.The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility.TRPV1 receptor was involved in the regulation of gastric motility of EAS.

View Article: PubMed Central - PubMed

Affiliation: Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie, Dongzhimennei, Beijing 100700, China.

ABSTRACT
The aim of this study was to explore the "intensity-response" relationship between EAS and the effect of gastric motility of rats and its underlying peripheral neural mechanism by employing ASIC3 knockout (ASIC3-/-), TRPV1 knockout (TRPV1-/-), and C57BL/6 mice. For adult male Sprague-Dawley (n = 18) rats, the intensities of EAS were 0.5, 1, 3, 5, 7, and 9 mA, respectively. For mice (n = 8 in each group), only 1 mA was used, by which C fiber of the mice can be activated. Gastric antrum motility was measured by intrapyloric balloon. Gastric motility was facilitated by EAS at ST36 and inhibited by EAS at CV12. The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA. In comparison with C57BL/6 mice, the facilitatory effect of ST36 and inhibitive effect of CV12 in ASIC3-/- mice decreased, but the difference was not statistically significant (P > 0.05). However, these effects in TRPV1-/- mice decreased significantly (P < 0.001). The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility. TRPV1 receptor was involved in the regulation of gastric motility of EAS.

No MeSH data available.


Related in: MedlinePlus

Gastric motility in response to 1 mA EAS at CV12 in three groups of mice. (a) showed representative examples of the alterations of gastric contraction wave induced by 1 mA EAS at CV12. (b), (c), and (d) displayed comparison of the inhibitory effects of 1 mA EA at CV12 on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (C57BL/6, n = 8; ASIC3−/−, n = 8; TRPV1−/−, n = 8; *P < 0.05, ***P < 0.001 versus C57BL/6).
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fig4: Gastric motility in response to 1 mA EAS at CV12 in three groups of mice. (a) showed representative examples of the alterations of gastric contraction wave induced by 1 mA EAS at CV12. (b), (c), and (d) displayed comparison of the inhibitory effects of 1 mA EA at CV12 on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (C57BL/6, n = 8; ASIC3−/−, n = 8; TRPV1−/−, n = 8; *P < 0.05, ***P < 0.001 versus C57BL/6).

Mentions: The previous data showed that there existed a possibility of “intensity-response” relationship between stimulation and effects of gastric motility. We speculated that the EAS with intensities of activation Aδ and C fiber played important roles for modulating gastric motility. According to the threshold of C fiber of mice [21], 1 mA was administrated. EAS with 1 mA at ST36 induced facilitatory effects of gastric motility, and the amplitude as well as integral increased by 45.8 ± 1.7% and 57.2 ± 3.1%, respectively, in C57BL/6 mice. Notably, the facilitatory effects partly diminished in ASIC3 and TRPV1 knockout mice (Figures 3 and 4). The facilitatory effects reduced a little in ASIC3−/− mice but markedly in TRPV1−/− mice (amplitude: 20.6 ± 2.1%; integral: 34.6 ± 3.2%, P < 0.001, Figures 3(b) and 3(c)) compared with that in C57BL/6 mice so did the inhibitory effects by CV12 in ASIC3−/− and TRPV1−/− mice (P < 0.001, Figures 4(b) and 4(c)). The frequency increased by 17.5 ± 3.8% in C57BL/6 mice via 1 mA EAS at ST36. The facilitatory effects on frequency slightly reduced in ASIC3−/− mice but significantly in TRPV1−/− mice (frequency: 5 ± 2.1%, P < 0.05, Figure 3(d)) so did the inhibitory effects by CV12 in ASIC3−/− and TRPV1−/− mice (P < 0.05, Figure 4(d)). Taken together, these observations provided direct evidence for the role of TRPV1, rather than ASIC3, in EAS-mediated facilitatory and inhibitory effects on gastric motility.


"Intensity-response" effects of electroacupuncture on gastric motility and its underlying peripheral neural mechanism.

Su YS, He W, Wang C, Shi H, Zhao YF, Xin JJ, Wang XY, Shang HY, Hu L, Jing XH, Zhu B - Evid Based Complement Alternat Med (2013)

Gastric motility in response to 1 mA EAS at CV12 in three groups of mice. (a) showed representative examples of the alterations of gastric contraction wave induced by 1 mA EAS at CV12. (b), (c), and (d) displayed comparison of the inhibitory effects of 1 mA EA at CV12 on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (C57BL/6, n = 8; ASIC3−/−, n = 8; TRPV1−/−, n = 8; *P < 0.05, ***P < 0.001 versus C57BL/6).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3713365&req=5

fig4: Gastric motility in response to 1 mA EAS at CV12 in three groups of mice. (a) showed representative examples of the alterations of gastric contraction wave induced by 1 mA EAS at CV12. (b), (c), and (d) displayed comparison of the inhibitory effects of 1 mA EA at CV12 on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (C57BL/6, n = 8; ASIC3−/−, n = 8; TRPV1−/−, n = 8; *P < 0.05, ***P < 0.001 versus C57BL/6).
Mentions: The previous data showed that there existed a possibility of “intensity-response” relationship between stimulation and effects of gastric motility. We speculated that the EAS with intensities of activation Aδ and C fiber played important roles for modulating gastric motility. According to the threshold of C fiber of mice [21], 1 mA was administrated. EAS with 1 mA at ST36 induced facilitatory effects of gastric motility, and the amplitude as well as integral increased by 45.8 ± 1.7% and 57.2 ± 3.1%, respectively, in C57BL/6 mice. Notably, the facilitatory effects partly diminished in ASIC3 and TRPV1 knockout mice (Figures 3 and 4). The facilitatory effects reduced a little in ASIC3−/− mice but markedly in TRPV1−/− mice (amplitude: 20.6 ± 2.1%; integral: 34.6 ± 3.2%, P < 0.001, Figures 3(b) and 3(c)) compared with that in C57BL/6 mice so did the inhibitory effects by CV12 in ASIC3−/− and TRPV1−/− mice (P < 0.001, Figures 4(b) and 4(c)). The frequency increased by 17.5 ± 3.8% in C57BL/6 mice via 1 mA EAS at ST36. The facilitatory effects on frequency slightly reduced in ASIC3−/− mice but significantly in TRPV1−/− mice (frequency: 5 ± 2.1%, P < 0.05, Figure 3(d)) so did the inhibitory effects by CV12 in ASIC3−/− and TRPV1−/− mice (P < 0.05, Figure 4(d)). Taken together, these observations provided direct evidence for the role of TRPV1, rather than ASIC3, in EAS-mediated facilitatory and inhibitory effects on gastric motility.

Bottom Line: The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA.The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility.TRPV1 receptor was involved in the regulation of gastric motility of EAS.

View Article: PubMed Central - PubMed

Affiliation: Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie, Dongzhimennei, Beijing 100700, China.

ABSTRACT
The aim of this study was to explore the "intensity-response" relationship between EAS and the effect of gastric motility of rats and its underlying peripheral neural mechanism by employing ASIC3 knockout (ASIC3-/-), TRPV1 knockout (TRPV1-/-), and C57BL/6 mice. For adult male Sprague-Dawley (n = 18) rats, the intensities of EAS were 0.5, 1, 3, 5, 7, and 9 mA, respectively. For mice (n = 8 in each group), only 1 mA was used, by which C fiber of the mice can be activated. Gastric antrum motility was measured by intrapyloric balloon. Gastric motility was facilitated by EAS at ST36 and inhibited by EAS at CV12. The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA. In comparison with C57BL/6 mice, the facilitatory effect of ST36 and inhibitive effect of CV12 in ASIC3-/- mice decreased, but the difference was not statistically significant (P > 0.05). However, these effects in TRPV1-/- mice decreased significantly (P < 0.001). The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility. TRPV1 receptor was involved in the regulation of gastric motility of EAS.

No MeSH data available.


Related in: MedlinePlus