Table Of ContentYing Xia
Xiaoding Cao
Gencheng Wu
Jieshi Cheng
Acupuncture Therapy for Neurological Diseases:
A Neurobiological View
Ying Xia
Xiaoding Cao
Gencheng Wu
Jieshi Cheng
Acupuncture Therapy for
Neurological Diseases:
A Neurobiological View
With 87 figures
(cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3) (cid:3)
Editors:
Prof. Ying Xia Prof. Gencheng Wu
Yale University School of Medicine Department of Integrative Medicine and
New Haven, CT 06520, USA Neurobiology and
Email: [email protected] State Key Laboratory of Medical Neurobiology
Shanghai Medical College of Fudan University
Shanghai 200032, P.R. China
Email: [email protected]
Prof. Xiaoding Cao
State Key Laboratory of Medical
Neurobiology and Prof. Jieshi Cheng
Department of Integrative Medicine and State Key Laboratory of Medical Neurobiology and
Neurobiology Department of Integrative Medicine and
Shanghai Medical College of Fudan Neurobiology
University Shanghai Medical College of Fudan University
Shanghai 200032, P.R. China Shanghai 200032, P.R. China
Email: [email protected] Email: [email protected]
ISBN 978-7-302-21108-2
Tsinghua University Press, Beijing
ISBN 978-3-642-10855-6 e-ISBN 978-3-642-10857-0
Springer Heidelberg Dordrecht London New York
Library of Congress Control Number: 2009940572
© Tsinghua University Press, Beijing and Springer-Verlag Berlin Heidelberg 2010
This work is subject to copyright. All rights are reserved, whether the whole or part of the material is
concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation,
broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of
this publication or parts thereof is permitted only under the provisions of the German Copyright Law of
September 9, 1965, in its current version, and permission for use must always be obtained from
Springer-Verlag. Violations are liable to prosecution under the German Copyright Law.
The use of general descriptive names, registered names, trademarks, etc. in this publication does not
imply, even in the absence of a specific statement, that such names are exempt from the relevant
protective laws and regulations and therefore free for general use.
Cover design: Frido Steinen-Broo, EStudio Calamar, Spain
Printed on acid-free paper
Springer is part of Springer Science+Business Media (www.springer.com)
Figure 3.2(cid:3) Diagram showing the damaged areas in spinal cord of the patient
with Tabes dorsalis and Syringomyelia.
Figure 6.5(cid:3) Droperidol (Dro) further enhances the EA-induced increase in
(cid:80)-opioid receptor density. The (cid:80)-opioid receptor was labeled with 3H-ohmefentany
(OMF), and the rats were divided into four groups. For Dro(cid:14)EA group, 10 min after
the injection of Dro (1.25 mg/kg, i.p.), EA stimulation was given at Zusanli (ST-36)
and Kunlun (BL-60) acupoints lasting for 20 min. For the NS(cid:14)EA group, normal
saline (NS) administration was followed by EA treatment. The rats in the Dro or
NS group received i.p. injection of Dro or NS, respectively, as the control. In the
autoradiographic images, the red color indicates higher density of the opioid receptors,
while the blue indicates lower density. Note that when EA was applied alone (NS(cid:14)EA),
(cid:80)-like binding sites were significantly increased in the telencephalon (caudate nucleus,
accumbens, septum, preoptic area), diencephalon (medial nuclei of thalamus and
hypothalamus, reticular nucleus of thalamus, amygdala), and midbrain [periaqueductal
gray (PAG), etc.], when compared with the NS group. When Dro was combined with
EA (Dro(cid:14)EA), the increase in (cid:80)-like binding sites in the abovementioned nuclei
was higher than that observed in the EA(cid:14)NS group. Upper-left: NS group; Upper-right:
Dro group; Lower-left: NS(cid:14)EA group; Lower-right: Dro(cid:14)EA group.
Figure 7.1 Countries where clinical acupuncture is practiced for pain relief.
Note that acupuncture analgesia is used in most of the major countries and regions
all over the world.
Figure 8.2 Peripheral inflammatory pain model induced by injecting CFA into
the hand paw of rats.
Figure 9.2 Infarction after MCAO. (a), A clot blocks the blood flow of MCA and
induces infarction, which is represented by grey color. (b) and (c), Triphenyltetrazolium
chloride (TTC) staining after transient MCAO and reperfusion. Infarction is
represented by pale white color. (b) shows the whole brain tissue. (c) shows the
coronal brain section.
Figure 9.4 The decrease in the ischemic infarction volume after EA treatment.
The rat brains were cut into a series of 2 mm thick slices and stained using TTC.
Left column, EA plus ischemia (MCAO). Right column, ischemia alone.
Figure 13.3 Schematic pathways involved in the acupuncture-induced effect
on immune system.
Figure 13.4 Schematic representation of the initiation pathway of immune
response within brain. Stimulators like virus, bacteria, dead cells or debris, and toxic
central nervous system proteins, could be recognized by the immune competent cells,
and subsequently, immune responses are initiated. In this process, proinflammatory
cytokines, chemokines, and neurotransmitters are found to be involved.
Figure 14.2 Effects of EA on maturation and exfoliation of rat vaginal
epithelium(cid:117)200.This picture shows the maturation and exfoliation of rat vaginal
epithelium with HE staining under optical microscope. Some matured exfoliative
epithelium and white blood cells were detected in the vaginal smears of INT rats during
preestrus, but no change in the vaginal exfoliative epithelium of INT rats following EA
treatment was observed. Some epithelium debris were detected in the vaginal smears
of OVX rats 4 weeks after ovariectomy, but the matured, exfoliative epidermic
keratinocytes reappeared in the vaginal smears of OVX(cid:14)EA rats after three
successive EA treatments.
Figure 15.2 The GnRH neurons around organum vasculosum of the lamina
terminalis (OVLT) of the INT, INT(cid:14)EA, OVX, and OVX(cid:14)EA rats. Female
Sprague-Dawley rats (180(cid:16)200 g), with regular 4-day estrus cycles were divided
into four groups: intact (INT), intact with EA (INT(cid:14)EA), ovariectomized (OVX),
and ovariectomized with EA (OVX(cid:14)EA). The acupoints employed were Guanyuan
(RN-4), Zhongji (RN-3), Zigongxue (EXTRA-22), and Sanyinjiao (SP-6). The
stimulation was generated by an EA apparatus and lasted for 30 min (8:00(cid:16)
10:00 AM), once a day, total for 3 days. The stimulation parameters were 2 mA of
density and a low-burst frequency of 3 Hz. The upper picture shows the light micro-
graphs of the GnRH immunoreactive neurons around OVLT by immunohistochemical
method (ABC). The GnRH immunoreactive neurons were detected by the
polyclonal antibody. The numbers of GnRH neurons in the all-continuous slices
was expressed as mean(cid:114) SEM (n(cid:32)6 per group) in each column, indicated in the
lower panel. *p<0.05 vs. INT and INT(cid:14)EA; **p<0.05 vs. OVX.
Note that EA may modulate the synthesis and release of central GnRH at the
molecular level, and also enhance the pituitary GnRH—R mRNA level, which
may be the central mechanism by which acupuncture regulates the dysfunction of
hypothalamic-pituitary-adrenal axis (HPAA).
Figure 17.1 EA attenuates the decrease in the hippocampal progenitor cell proli-
feration in the adult rats exposed to CUS. Panels (a) (b), and (c) are representative
photographs showing the distribution of BrdU-labeled cells in the hippocampus
from the groups of Control (a), Stress (b), and Stress(cid:14)EA (c). The BrdU-labeled
cells, as indicated by arrows, appear in pairs or clusters in the subgranular zone
(SGZ) of the DG. Under a 40(cid:117) with a 100(cid:117) zoom magnification, individual cells
in the clusters are clearly visualized (d). The BrdU-labeled cells in the SGZ were
counted under high magnification. Panel (e) shows the number of BrdU-labeled
cells in the SGZ of rats. The results are expressed as the estimated mean total
number ((cid:114)SEM). **p<0.01 for the stress group vs. the control group; $$p<0.01
for the Stress(cid:14)EA group vs. the Stress(cid:14)sham EA group.
