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Evidence-Based Complementary and Alternative Medicine
Volume , Article ID , pages
http://dx.doi.org/.//
Research Article
‘‘Intensity-Response’’ Effects of Electroacupuncture on Gastric
Motility and Its Underlying Peripheral Neural Mechanism
Yang-Shuai Su,1Wei He,1Chi Wang,2Hong Shi,1Yu-Feng Zhao,3Juan-Juan Xin,1
Xiao-Yu Wang,1Hong-Yan Shang,1Ling Hu,1Xiang-Hong Jing,1and Bing Zhu1
1Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie,
Dongzhimennei, Beijing 100700, China
2Department of Gastroenterology, Peking University First Hospital, 6 Xishiku Street, Beijing 100034, China
3Institute of Basic and Clinic Medicine, China Academy of Chinese Medical Sciences, 16 Nanxiaojie,
Dongzhimennei, Beijing 100700, China
Correspondence should be addressed to Xiang-Hong Jing; xianghongjing@hotmail.com and Bing Zhu; zhubing@mail.cintcm.ac.cn
Received March ; Revised June ; Accepted June
Academic Editor: Yi-Hung Chen
Copyright © Yang-Shuai Su et al. is is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
e aim of this study was to explore the “intensity-response” relationship between EAS and the eect of gastric motility of rats
and its underlying peripheral neural mechanism by employing ASIC knockout (ASIC−/−), TRPV knockout (TRPV−/−), and
CBL/ mice. For adult male Sprague-Dawley (=18)rats,theintensitiesofEASwere.,,,,,andmA,respectively.
For mice (=8in each group), only mA was used, by which C ber of the mice can be activated. Gastric antrum motility was
measured by intrapyloric balloon. Gastric motility was facilitated by EAS at ST and inhibited by EAS at CV. e half maximal
facilitation intensity of EAS at ST was .–.mA, and the half maximal inhibitory intensity of EAS at CV was .mA. In
comparison with CBL/ mice, the facilitatory eect of ST and inhibitive eect of CV in ASIC−/−mice decreased, but the
dierence was not statistically signicant ( > 0.05). However, these eects in TRPV−/−mice decreased signicantly ( < 0.001).
e results indicated that there existed an “intensity-response” relationship between EAS and the eect of gastric motility. TRPV
receptor was involved in the regulation of gastric motility of EAS.
1. Introduction
Acupuncture therapy, as a traditional Chinese medicinal
treatment, has been widely used in clinical practice in oriental
countries. And it has been more accepted by practitioners
and patients worldwide aer its therapeutic eects for the
treatments of postoperative dental pain, nausea, and vomiting
have been conrmed by NIH in []. Electroacupuncture
(EA) is a modication of conventional manual acupuncture
to stimulate acupoints with electrical current. It appears to
induce more consistently reproducible eects in both clinical
and animal researches than manual acupuncture [].
During the last decades, a large number of studies have
been performed to investigate the eects of acupuncture on
gastrointestinal secretion, motility, and gastric myoelectrical
activity [–]. Some regular responses of gastrointestinal tract
induced by acustimulation have been observed in various
studies. In animal models, acupuncture at hindlimb has
been reported to accelerate delayed gastric emptying [],
restore impaired gastric accommodation in vagotomized
dogs [], and relax the gastric fundus in rats []viathe
parasympathetic pathway, whereas application of acupunc-
ture at the abdomen was more likely to inhibit gastrointestinal
motility [,] via the sympathetic pathway. Most studies
have mainly focused on whether acupuncture treatment is
eective for restoring gastrointestinal disorders. However,
few were performed to explore the “intensity-response”
relationship between electroacupuncture stimulation (EAS)
and the eect. In the present paper, according to the threshold
of activating peripheral III (A)andIV(C)primaryaerent
bers [], EAS with dierent intensities was introduced to
reveal the “intensity-response” eects between EAS and the
eect of gastric motility.
Evidence-Based Complementary and Alternative Medicine
Previous studies showed that Aand Amechanical
receptors, as well as C-polymodal receptors, played important
roles in the acupuncture stimulation perception [–]. But
what aerent bers mediate the regulatory eect of EAS on
the internal organs was ignored. Acid sensing ion channel
(ASIC) is a member of the DEG/ENaC family which is
knowntomediatemechanicalresponsiveness[]andlocat-
ed mainly in Aprimary aerent bers innervating the skin
and muscle [,]. Transient receptor potential vanilloid
(TRPV) belongs to TRPV subfamily, which is expressed in
sensory AandCbers.Itcanbeactivatedbycapsaicin,
noxious heat, low PH, and voltage and closely related to
noxious physical detection [–]. In our previous study,
these two knockout mice have been utilized to observe the
eect of EAS on mechanical and thermal pain thresholds,
which showed that both EA and thermal stimulation of the
right ST can raise mechanical and thermal pain thresholds
in TRPV−/−and CBL/ mice, but stimulation should be
more stronger in TRPV−/−mice [].
In the present study, both ASIC knockout (ASIC−/−)
mice and TRPV knockout (TRPV−/−) mice were employed
to establish dysfunction of Aand A/C aerent ber mice
models, respectively, in order to investigate the roles of A
and A/C bers in the EAS-modulated gastric motility.
2. Materials and Methods
2.1. Animal Preparation. Male Sprague-Dawley (SD) rats
(=18), weighing – g, were purchased from Institute
of Animal, Academy of Chinese Medical Sciences. Male
ASIC−/−mice (=8), TRPV−/−mice (=8), and
CBL/J mice (=8),weighing–g,werepurchased
from Jackson Lab (USA) and bred at the China Academy of
Chinese Medical Science Animal Care Facility. e animals
were housed under a h light/dark with free access to food
and water. All animals were treated according to the Guide for
Use and Care of Medical Laboratory Animals from Ministry
of Public Health of People’s Republic of China.
2.2. Gastric Motility Recording. e animals were fasted over-
night with free access to water. For anesthesia, % urethane
(.–. g/kg, via intraperitoneal route) was administered.
About h aer the urethane administration, the animals
were under deep anesthesia, and the trachea was cannulated
but not immobilized to keep respiratory tract unobstructed.
A catheter was inserted into one of the jugular veins for
infusion. A small longitudinal incision was made in the duo-
denum about cm from the pylorus. A small balloon made
of exible condom rubber was inserted via incision of the
duodenum into the pyloric area of rat and kept in position by
tying the connecting catheter to the duodenum. And another
catheter (inner diameter of mm) was also inserted into
the same hole by incision in order to drain digestive juices
secreted from stomach. e balloon was lled with about .–
. mL warm water to keep pressures at about mmH2O.
Fortheoperationofthemice,asmallerballoonlledwith
.–. mL warm water was inserted into the pyloric area
to keep the pressures at about mmH2O.
Pressure in the balloon was measured by a transducer
through a thin polyethylene tube (. mm in outer diame-
ter) and then input into a polygraph amplier (NeuroLog,
NLD). e signal was captured online and analyzed o-
line using a data acquisition system (Power-Lab/s, AD
Instruments) and Chart . soware. Demifasting gastric
motor activity was recorded as a control for at least min
before any stimulation. e gastric motility induced by EAS
was compared with the background activity in terms of
average amplitude (the average dierence between the cyclic
maxima and minima in the selected cycles), integral (returns
the integral of the selection, calculated as the sum of the
data points multiplied by the sample interval), and frequency
(per minute) of gastric contraction waves. Systemic blood
pressure and heart rate were continuously monitored by using
of BIOPAC data acquisitionsystem (MP, USA), and rectal
temperature kept constantly around ∘C by a feedback-
controlled heating blanket (DC, USA).
Gastric motility during and aer EAS was compared with
background activity. If the change rates of gastric motility
during or aer EAS were –% of the basal activity,
the response was then considered to have an excitatory or
inhibitory eect. e rst EA stimulus was applied when
gastric motility wave maintained stable, usually at about
minutes aer the surgical procedure. Dierent intensities of
EAS, including . mA (<TA𝛿), mA (<TA𝛿), mA (>TA𝛿,
<TC), mA (>TC), mA (>TC), and mA (>TC), were
applied at ST or CV in an ascending order. e latter
stimuluscanonlybeappliedwhenthegastricmotility
recovered to control state. e background gastric activity
and gastric activity during and aer EAS were recorded
continuously, s for each session.
2.3. Electroacupuncture Stimulation (EAS) of CV12 and ST36.
Rats were randomly divided into ST group (=9)and
CV group (=9). A needle (. mm in diameter) was
inserted into the skin and its underlying muscles at acupoints
Zhongwan (CV) and Zusanli (ST) on the body. CV was
located at center of abdomen, in middle line of the body. ST
was located bilaterally at the anterior tibia muscles near the
knees.EASwasperformedatunilateralSTorCVfor
s. A pair of noninsulated needle electrodes inserted into
the skin of the acupoints with .cm distance. e needles
were connected to an electronic stimulator (SEN-, Nihon
Kohden) with the parameters as follows: duration: ms, pulse
frequency: Hz. For rats, the current intensities were ., ,
, , , and mA, respectively. For mice, only mA EAS was
administrated.
2.4. Statistical Analysis. Changes in the average amplitude
andintegralwerecalculatedaccordingto(thevalueduring
EAS-the value pre EAS)/the value pre EAS ×%. e data
obtainedbeforeandaertreatmentinthesamegroupor
dierent group was compared statistically by a paired -test
or unpaired -test. < 0.05 was considered as a statistical
signicance. All data are expressed as mean ±SE.
Evidence-Based Complementary and Alternative Medicine
e data was tted with (), where is set to be , is
set to be , and issettobe:
=
1 + exp (−
)∗.()
3. Results
3.1. Gastric Motility under Resting Condition. e gastric
motility of the rats and mice was detected by recording the
intragastric pressure. When the intrapyloric balloon pressure
was increased to about – mmH2O, the rhythmic waves
of contractions in pyloric area were observed. With regard
to gastric motor characteristics, both the changes of intra-
gastric pressure and rhythmic contraction were noteworthy.
Generally, the intragastric pressure represents the index of
gastric tone motility, and rhythmic contraction represents
gastric peristalsis induced by circular muscle contractions,
similartoslowwaveofgastricmotoractivity.epressure
was maintained at about mmH2O as baseline by expand-
ing the volume of the balloon with warm water, rhythmic
contractions occurred at a rate of four to six per minute, and
these rhythmically gastric contractions were recorded in both
the rats and mice.
3.2. Facilitatory Eect of Gastric Motility Induced by ST36
and Its Intensities Response Eects of the Rats. EAS at ST
induced facilitatory eects which were related to the intensi-
ties. Figure (a) showed typical responses of gastric motility
following EAS with various intensities for s. Figures (b)
and (c) summarized the responses obtained from all
tested rats. It should be noted that when the stimulation was
less than mA, there was no signicant response of gastric
motility (amplitude changes: . mA: . ±.%, mA: .
±.%, > 0.05)(integralchanges:.mA:.±.%,
mA: . ±.%, > 0.05). However, mA, mA, mA,
and mA EAS at ST elicited a signicant enhancement on
the amplitude and integral of gastric contraction compared
with the background activities (amplitude changes: mA:
. ±.%, mA: . ±.%, mA: . ±.%, mA:
. ±.%, < 0.01, < 0.001)(integralchanges:
mA: . ±.%, mA: . ±.%, mA: . ±.%,
mA: . ±.%, < 0.001). e facilitation of EAS at
ST appeared from a low intensity with an EC50 value of
approximately . mA for amplitude (Figure (b))and.mA
for integral (Figure (c)), which means that EAS with .–
. mA can obtain % of the maximum facilitatory eect.
For the intensity of EAS above mA, the response eciency
did not increase correspondingly as intensities increasing,
which indicated that the eects may hit a “plateau region”
when the stimulating intensity reached to a certain level.
Figure (d) illustrated the impact of EAS at ST on the
frequency of gastric motility. Intensity of EAS lower than
mA failed to produce any signicant response (frequency
changes: . mA: . ±./min, mA: . ±./min,
> 0.05),whilemA,mA,mA,andmAEASat
ST induced signicant enhancement on the frequencies
of gastric motility compared with the background activ-
ities (frequency changes: mA: . ±./min, mA:
. ±./min, mA: . ±./min,mA:.±
./min, < 0.05, < 0.01). e maximal facilitatory
response of the frequency appeared as the intensities reached
to mA.
3.3. Inhibitory Eect of Gastric Motility Induced by CV12
and Its Intensities Response Eect of the Rats. EAS at CV
induced inhibitory eects which were also related to the
intensities. Figure (a) showed typical responses of gastric
motility following EAS with dierent intensities for s, and
Figures (b) and (c) summarized the responses obtained
from all tested rats. EAS with all the intensities at CV
induced signicant inhibition eects on the amplitudes and
integrals of gastric contraction (amplitude: . mA: −. ±
.%, < 0.05;mA:−. ±.%, mA: −. ±.%, mA:
−. ±%, mA: −. ±%, and mA: −. ±. % , <
0.01)(integral:.mA:−. ±.%, < 0.01;mA:−.
±.%, mA: −. ±%, mA: −. ±.%, mA: −.
±.%, and mA: −. ±.%, < 0.001). e inhibition
of EAS at CV appeared from a low intensity (. mA), with
IC50 value of approximately . mA for both amplitude and
integral (Figure (b)). is means that EAS with .mA can
obtain % of the maximum inhibitory eect. When the
intensity reached to mA, the response eciency did not
increase correspondingly. e “plateau region” also appeared
in the CV which induced the inhibitory eects.
Figure (d) displayed the impact of EAS on the frequency
of gastric motility by CV. Intensities of EAS lower than
mA had no signicant inuence on the frequencies (fre-
quency changes: . mA: −. ±./min, and mA: −.
±./min, > 0.05). But mA, mA, mA, and mA EAS
at CV induced a signicant inhibition on the frequency
of gastric motility compared with the background activities
(frequency changes: mA: −. ±./min, mA: −. ±
./min, mA: −. ±./min, and mA: −. ±./min,
< 0.01). e inhibitory response of the frequency was
pronetobemaximalwhentheintensityreachedtomA.
3.4. Facilitatory and Inhibitory Eects of EAS on Gastric
Motility Require ASIC3 and TRPV1 Receptors. e previous
data showed that there existed a possibility of “intensity-
response” relationship between stimulation and eects of
gastric motility. We speculated that the EAS with intensities
of activation Aand C ber played important roles for
modulating gastric motility. According to the threshold of C
ber of mice [], mA was administrated. EAS with mA
at ST induced facilitatory eects of gastric motility, and
the amplitude as well as integral increased by . ±.%
and . ±.%, respectively, in CBL/ mice. Notably, the
facilitatory eects partly diminished in ASIC and TRPV
knockout mice (Figures and ). e facilitatory eects
reduced a little in ASIC−/−mice but markedly in TRPV−/−
mice (amplitude: . ±.%; integral: . ±.%, <
0.001,Figures(b) and (c))comparedwiththatinCBL/
mice so did the inhibitory eects by CV in ASIC−/−and
TRPV−/−mice ( < 0.001,Figures(b) and (c)). e
frequency increased by . ±.% in CBL/ mice via mA
EAS at ST. e facilitatory eects on frequency slightly
reducedinASIC−/−mice but signicantly in TRPV−/−
Evidence-Based Complementary and Alternative Medicine
10
14
0123
1
3
5
7
9
EA ST36 (min)
0.5
(mA)
cmH2O
(a)
0.5 13579
0
20
40
60
80
100
Intensity (mA)
Increase in amplitude of gastric motility (%)
ST36
(b)
0.5 1 3 579
0
20
40
60
80
100
Intensity (mA)
Increase in integral (%)
ST36
(c)
0
0.25
0.5
0.75
1
Intensity (mA)
ST36
0.5
Increase in frequency of gastric motility (/min)
13579
∗
∗
∗
∗∗
(d)
F : Gastric motility in response to EAS at ST with dierent intensities in rats. (a) Representative examples of the alterations of gastric
contraction wave induced by dierent intensities of EAS at ST. (b), (c), and (d) displayed the facilitatory eects of EAS at ST on the
amplitude, integral, and frequency of gastric motility, respectively (=9;∗ < 0.05,∗∗ < 0.01, versus background activities).
mice (frequency: ±.%, < 0.05,Figure (d))sodidthe
inhibitory eects by CV in ASIC−/−and TRPV−/−mice
( < 0.05,Figure (d)). Taken together, these observations
provided direct evidence for the role of TRPV, rather than
ASIC, in EAS-mediated facilitatory and inhibitory eects on
gastric motility.
4. Discussion
In the present study, we investigated the “intensity-response”
relationship between EAS and the eect of gastric motility
in rats. And we rstly observed which aerent bers were
involved in the eect of EAS on gastric motility by using of
knockout mice. Our ndings strongly indicated the existence
of “intensity-response” eects of EAS on gastric motility. EAS
at ST induced facilitatory eects which were related to
the intensities. Aer data tting, the EC50 (the half maximal
facilitation intensity) of EAS at ST, was .–. mA, which
was near the threshold of Aber. EAS at CV displayed
inhibitory eects which were also related to the intensities.
e IC50 (the half maximal inhibitory intensity) of EAS at
CV, was about . mA, which was also near the threshold of
Aber. ese data suggested that the activation of Aber
was important for EAS-modulated gastric motility. Further
study in ASIC and TRPV knockout mice showed that both
ASIC and TRPV receptors were involved in the eects of
EAS on gastric motility, but there was a quantity dierence
in the changes of gastric motility between ASIC and TRPV
knockout mice. TRPV played a more important role in the
eects of EAS.
Based on another experiment in our research group,
mA was strong enough to activate the C primary aerent
ber in mice. e dierent gastric responses induced by
mA EAS between ST and CV were mainly caused by
diverse somatoautonomic reexes; that is, the facilitatory
eectofEAatSTwasmediatedviatheparasympathetic
pathway, whereas the inhibitory eect of EA at abdomen
wasreasonedtobeattributedtothesympatheticpathway.
Evidence-Based Complementary and Alternative Medicine
0.5
0123
1
3
5
7
9
EA CV12 (min)
(mA)
10
14
cmH2O
(a)
0.5 1 3 5 7 9
Intensity (mA)
Increase in amplitude of gastric motility (%)
CV12
−100
−80
−6 0
−4 0
−20
0
(b)
0.5 1 3 5 7 9
Intensity (mA)
Increase in integral (%)
CV12
−100
−80
−60
−40
−20
0
(c)
Intensity (mA)
CV12
Increase in frequency of gastric motility (/min)
0.5 13579
−4
−3
−2
−1
0
∗∗∗
∗∗∗
∗∗∗
∗∗∗
(d)
F : Gastric motility in response to EAS at CV with dierent intensities in rats. (a) Representative examples of the alterations of
gastric contraction wave induced by dierent intensities of EAS at CV. (b), (c), and (d) displayed the inhibitory eects of EAS at CV on
the amplitude, integral, and frequency of gastric motility, respectively (=9;∗∗∗ < 0.001 versus background activities).
e involvement of the opioidergic pathway has also been
frequently reported [,]. EA was more likely to activate
various aerent bers of rats including groups II-III [],
groups III-IV [], or groups II–IV []. Recent study showed
that the subepidermal nerve bers showed the colocalization
of TRPV with peripherine, a marker for the C and Abers.
Relationship between TRPV and eects of acupuncture was
further investigated recently. Our previous study suggested
an involvement of TRPV receptors in acupuncture analgesia
[].Wangetal.showedthatEAatSTandSTreduces
zymosan-induced colorectal hypersensitivity through reg-
ulating TRPV expression []. Moreover, the expression
of TRPV in subepidermal nerve bers was signicantly
increased by EAS at BL, which indicated that TRPV
may play a role in local eect of the EA []. According
to the result of this study, the modulatory eects of EAS
at both ST and CV were barely changed in ASIC−/−
mice compared with CBL/ mice. However, the potency
of stimulating these two acupoints decreased signicantly
in TRPV−/−mice. ese results suggested that Aand C
ber were more critical than Aber in the eects of EA-
modulated gastric motility. In another somatovisceral reex
study, Noguchi et al. revealed that to decrease duodenal
motilities, EAS to the abdomen needed to be strong enough
to excite group IV (C) bers of intercostal nerves. To increase
motilities, EAS to the hindpaw needs to be strong enough
to excite the higher threshold group III (A)bersoftibial
nerves. eir results also indicated the critical roles of A
and C primary aerent bers in eective regulation of EAS on
visceral organ, which were quite similar to our results [].
It is generally believed that acupuncture at dierent
acupoints produces dierent eects, and the site-specic
inhibitory or facilitatory eects of acupuncture on gastric
motility had already been proposed [,,]. In the present
Evidence-Based Complementary and Alternative Medicine
0123
1mA EA ST36 (min)
10
14
C57BL/6
ASIC3−/−
TRPV1−/−
cmH2O
(a)
0
20
40
60
Increase in amplitude of gastric motility (%)
ST36
∗∗∗
(b)
0
14
28
42
56
70
ST36
Increase in integral (%)
C57BL/6
ASIC3−/−
TRPV1−/−
∗∗∗
(c)
0
6
12
18
24
ST36
Increase in frequency of gastric motility (%)
C57BL/6
ASIC3−/−
TRPV1−/−
∗
(d)
F : Gastric motility in response to mA EAS at ST in three groups of mice. (a) Representative examples of the alterations of gastric
contraction wave induced by mA EAS at ST. (b), (c), and (d) displayed the comparison of the facilitatory eects of mA EAS at ST
on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (CBL/, =8;ASIC−/−,=8;
TRPV−/−,=8;∗ < 0.05,∗∗∗ < 0.001 versus CBL/).
study, we found that EAS with dierent intensities at ST
induced facilitatory responses of gastric motility, whereas
EAS at CV produced an inhibitory impact on gastric
motility. e consistent results have been reported in previous
studies [,]. e facilitatory eects of EAS at ST, as well
as inhibition eects of EAS at CV, ranged from % to %
approximately. e eects reached saturation when the inten-
sitygottoacertainlevel.ItwasalsomanifestedthatEAShada
relative narrow band control for the gastric motility and EAS
modulation was a kind of self-limiting and self-regulation to
promote the regulation of homeostasis of the body, which
demonstrated that EAS modulation is a safe therapy.
5. Conclusion
ere existed “intensity-response” relationship between stim-
ulation and eects on gastric motility. TRPV receptor was
involved in the regulation process of EAS. It is necessary
to activate Aber to get remarkable modulatory eects,
and these eects tended to maximization when C ber was
activated.
Authors’ Contribution
e experiments were done by Yang-Shuai Su, Wei He, and
Chi Wang, and they contributed equally to the work. Hong
Shi, Hongyan Shang, and Juanjuan Xin were responsible for
the mice identifying. Yufeng Zhao and Ling Hu provided
advice on the statistical analyses and data interpretation.
Yangshuai Su, Xianghong Jing, and Wei He draed and
nalized the paper. Xianghong Jing and Bing Zhu were
responsible for the conception, design, and overseeing the
implementation of the study.
Evidence-Based Complementary and Alternative Medicine
0123
10
14
C57BL/6
ASIC3−/−
TRPV1−/−
1mA EA CV12 (min)
cmH2O
(a)
Increase in amplitude of gastric motility (%)
CV12
0
−20
−40
−60
∗∗∗
(b)
CV12
Increase in integral (%)
C57BL/6
ASIC3−/−
TRPV1−/−
∗∗∗
0
−14
−28
−42
−56
−70
(c)
CV12
Increase in frequency of gastric motility (%)
C57BL/6
ASIC3−/−
TRPV1−/−
∗
0
−10
−20
−30
−40
(d)
F : Gastric motility in response to mA EAS at CV in three groups of mice. (a) showed representative examples of the alterations of
gastric contraction wave induced by mA EAS at CV. (b), (c), and (d) displayed comparison of the inhibitory eects of mA EA at CV
on the amplitude, integral, and frequency of gastric motility, respectively, among three groups of mice (CBL/, =8;ASIC−/−,=8;
TRPV−/−,=8;∗ < 0.05,∗∗∗ < 0.001 versus CBL/).
Conflict of Interests
All the authors declare that they have no conict of interests.
Acknowledgments
isworkwassupportedbyNationalKeyBasicResearchPro-
gram (nos. CB and CB), National
Natural Science Foundation of China (), and Beijing
Natural Science Foundation ().
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