中药薏苡仁和100Hz电针干预脊髓半横断性大鼠可降低损伤后胶质纤维酸性蛋白表达

实验建立正常对照组、假手术组、高低频电针组和中药薏苡仁干预组,横断T10左半侧的脊髓损伤模型大鼠,4h后使用5,100Hz电针刺激环跳(GB30)、足三里(ST 36)、至阳(DU9)及悬枢(DU5)或腹腔注射0.4μL中药薏苡仁粗提液(与生药比例为1:1),连续8周,观察发现低高频电针刺激及薏苡仁治疗能改善脊髓组织损伤区域形态,促进运动诱发电位的恢复,抑制损伤区胶质纤维酸性蛋白表达,改善半横断性脊髓损伤大鼠运动功能,以100Hz电针刺激和薏苡仁干预效果明显。     

Rat hypothalamic arcuate neuron response in electroacupuncture-induced analgesia

Electroacupuncture (EA) effects on activity of arcuate neurons of the hypothalamus (ARH) and on magnitude of the digastric electromyogram (dEMG) in the jaw opening reflex were investigated, in both p-chlorophenylalanine pretreated and normal Wistar rats. EA stimulation (300-500 microA, 5 msec pulses, for 15 min) was delivered unilaterally to a meridian Ho-Ku point of anesthetized rats at 3, 45 and 100 Hz. In control animals, EA stimulation at 3, 45 or 100 Hz induced long-lasting suppression of the magnitude of the dEMG activity and changed the spontaneous firing rate of most of the ARH neurons: the rate either increased (type I) or decreased (type II). After low-frequency stimulation, there were significantly more type I neurons than type II; after high-frequency stimulation, there were significantly more type II neurons than type I. In serotonin-depleted rats, however, high-frequency stimulation suppressed dEMG activity only slightly and induced a smaller proportion of type II neurons.     

低、高频闭环电刺激对氯化铁癫痫模型大鼠治疗作用的比较

目的探讨低、高频闭环电刺激对氯化铁癫痫模型大鼠的治疗效果。方法给予SD大鼠头颅额、顶、枕部铺设硬膜外电极6枚,用立体定向方法在大鼠感觉运动皮质区注入氯化铁溶液,建立癫痫模型,分别给予低频刺激(1Hz)和高频刺激(100Hz),同时给予8小时脑电监测。分析大鼠8小时内发作总次数和发作总时间。结果低频和高频电刺激均能抑制大鼠的癫痫发作,而高频与低频刺激在治疗效果上无明显统计学差异。结论低频刺激为较佳的刺激方式。     

Electroacupuncture protects against CCK-induced acute pancreatitis in rats

OBJECTIVE: Electroacupuncture (EA) has been used to treat myalgia, adiposis and gastroenteropathy in Korea. EA as a complementary and alternative medicine has been accepted worldwide mainly for the treatment acute and chronic pain and inflammation. The aim of this study was to investigate the effects of EA on acute pancreatitis induced by cholecystokinin octapeptide (CCK) in rats. METHODS: Animals were divided into four groups: (1) a normal group; (2) a CCK-induced acute pancreatitis group; (3) a CCK-induced acute pancreatitis group treated with 100-Hz EA, and (4) a CCK-induced acute pancreatitis group treated with 2-Hz EA. High-frequency (100-Hz) and low-frequency EA (2-Hz) stimulations were applied to an acupoint equivalent to Zusanli (ST36) in rats, followed by 75 microg/kg CCK subcutaneously three times, after 1, 3 and 5 h. The entire procedure was repeated over 5 days. Repeated CCK treatment resulted in typical laboratory and morphological changes in experimentally induced pancreatitis. RESULTS: EA significantly decreased the pancreatic weight/body weight ratio in CCK-induced acute pancreatitis, increased the pancreatic levels of HSP60 and HSP72, and decreased the beta-amylase and lipase levels associated with CCK-induced acute pancreatitis. Furthermore, the release of ACTH was increased in the blood serum of the EA-treated group. CONCLUSION: EA may have protective effects against CCK-induced acute pancreatitis through the release of ACTH.     

Effect of acupuncture on pubertal development of rats and rabbits at different developmental stages

Physiological and endocrine studies on sexual development in animals and effects of acupuncture on sexual development are limited. Therefore, we investigated the effect of electro-acupuncture (EA) on the arcuate nucleus (Arc) and release of gonadotropin-releasing hormone (GnRH) in animals at different developmental stages. In Experiment 1, EA stimulation (30 Hz) was performed for 30 min per day in EA group of rabbits for 48 days, while the control group (mature rabbits) was not given EA. Arc discharges in those two groups were measured after the 48-day treatment. Arc discharge was also measured in the pre-pubertal group (as control) without EA treatment. Then, all three groups were treated with transient EA for 30 min and Arc discharges were determined again. In Experiment 2, EA (3 Hz) at the same acupoints or non-acupoints as that in the rabbits was performed for 20 min per day in different developmental group of Sprague-Dawley rats for 10 days. GnRH mRNA expression in the hypothalamus of rats was determined using RT-PCR and real-time PCR. The serum sexual hormone, sperm count, and body weight was measured. The results showed that the Arc discharge (P<0.01), testosterone (T) (P<0.01) and sperm count (P<0.01) in male rabbits were reduced by repeated EA. However, the body weight of rabbits was not changed after EA compared to the control in Experiment 1. In Experiment 2, GnRH mRNA expression in rats of the early pubertal group (EPG) and adult group (AG) were significantly depressed after repeated EA at acupoints (P<0.01). The sexual hormones were negatively influenced by repeated EA during puberty. Sperm count was reduced significantly after repeated EA at time of puberty (P<0.01). Repeated EA did not influence body weight of rats (P>0.01) and structures of the gonadial tissues during development. The results suggested that repeated EA is a good option that can be considered for regulating the function of the hypothalamus-pituitary-gonad (HPG) axis during puberty.     

Electroacupuncture alleviates cerebral ischemia and reperfusion injury via modulation of the ERK1/2 signaling pathway

Electroacupuncture(EA) has anti-oxidative and anti-inflammatory actions,but whether the neuroprotective effect of EA against cerebral ischemia-reperfusion(I/R) injury involves modulation of the extracellular regulated kinase 1/2(ERK1/2) signaling pathway is unclear.Middle cerebral artery occlusion(MCAO) was performed in Sprague-Dawley rats for 2 hours followed by reperfusion for 24 hours.A 30-minute period of EA stimulation was applied to both Baihui(DU20) and Dazhui(DU14) acupoints in each rat(10 mm EA penetration depth,continuous wave with a frequency of 3 Hz,and a current intensity of 1–3 m A) when reperfusion was initiated.EA significantly reduced infarct volume,alleviated neuronal injury,and improved neurological function in rats with MCAO.Furthermore,high m RNA expression of Bax and low m RNA expression of Bcl-2 induced by MCAO was prevented by EA.EA substantially restored total glutathione reductase(GR),glutathione(GSH) and glutathione peroxidase(GSH-Px) levels.Additionally,Nrf2 and glutamylcysteine synthetase(GCS) expression levels were markedly increased by EA.Interestingly,the neuroprotective effects of EA were attenuated when ERK1/2 activity was blocked by PD98059(a specific MEK inhibitor).Collectively,our findings indicate that activation of the ERK1/2 signaling pathway contributes to the neuroprotective effects of EA.Our study provides a better understanding of the regulatory mechanisms underlying the therapeutic effectiveness of EA.     

Analgesic electrical stimulation of the hypothalamic arcuate nucleus: tolerance and its cross-tolerance to 2 Hz or 100 Hz electroacupuncture

Focal electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) for 5 min (1 session) produced a marked elevation of tail flick latency (TFL) to noxious heat in the pentobarbital-anesthetized rat. Repeated stimulation for a total of 11 sessions at 30 min intervals resulted in a gradual decline in the hypoalgesic action, and this tolerance may last for 7 days. Tolerance to the ARH analgesic stimulation reduced the analgesia produced by low (2 Hz) but not high (100 Hz) frequency electroacupuncture (EA); and tolerance to low frequency EA analgesia attenuated the ARH stimulation-produced analgesia without affecting high frequency EA analgesia. Alternatively, rats tolerant to high-frequency EA analgesia were still sensitive to either the ARH or low-frequency EA stimulation. These results suggest that the ARH stimulation and low-frequency EA administration produced analgesia via a common neural mechanism, supporting our hypothesis put forward previously that the ARH plays an important role in mediating low- but not high-frequency EA analgesia.     

Suppression of morphine withdrawal by electroacupuncture in rats: dynorphin and kappa-opioid receptor implicated

Our previous work has demonstrated that 100-Hz electroacupuncture (EA) or 100-Hz transcutaneous electrical nerve stimulation (TENS) was very effective in ameliorating the morphine withdrawal syndrome in rats and humans. The mechanism was obscure. (1) Rats were made dependent on morphine by repeated morphine injections (5-140 mg/kg, s.c., twice a day) for eight days. They were then given 100-Hz EA for 30 min 24 h after the last injection of morphine. A marked increase in tail flick latency (TFL) was observed. This effect of 100-Hz EA could be blocked by naloxone (NX) at 20 mg/kg, but not at 1 mg/kg, suggesting that 100-Hz EA-induced analgesia observed in morphine-dependent rats is mediated by kappa-opioid receptors. (2) A significant decrease of the concentration of dynorphin A (1-17) immunoreactivity (-ir) was observed in the spinal perfusate in morphine-dependent rats, that could be brought back to normal level by 100-Hz EA. (3) 100-Hz EA was very effective in suppressing NX-precipitated morphine withdrawal syndrome. This effect of EA could be prevented by intrathecal administration of nor-BNI (2.5 micrograms/20 microliters), a kappa-opioid receptor antagonist, or dynorphin A (1-13) antibodies (25 micrograms/20 microliters) administered 10 min prior to EA. In conclusion, while the steady-state spinal dynorphin release is low in morphine-dependent rats, it can be activated by 100-Hz EA stimulation, which may be responsible for eliciting an analgesic effect and ameliorating morphine withdrawal syndrome, most probably via interacting with kappa-opioid receptor at spinal level.     

Suppression of morphine withdrawal by electroacupuncture in rats: dynorphin and κ-opioid receptor implicated

Our previous work has demonstrated that 100-Hz electroacupuncture (EA) or 100-Hz transcutaneous electrical nerve stimulation (TENS) was very effective in ameliorating the morphine withdrawal syndrome in rats and humans. The mechanism was obscure. (1) Rats were made dependent on morphine by repeated morphine injections (5–140 mg/kg, s.c., twice a day) for eight days. They were then given 100-Hz EA for 30 min 24 h after the last injection of morphine. A marked increase in tail flick latency (TFL) was observed. This effect of 100-Hz EA could be blocked by naloxone (NX) at 20 mg/kg, but not at 1 mg/kg, suggesting that 100-Hz EA-induced analgesia observed in morphine-dependent rats is mediated by κ-opioid receptors. (2) A significant decrease of the concentration of dynorphin A (1–17) immunoreactivity (-ir) was observed in the spinal perfusate in morphine-dependent rats, that could be brought back to normal level by 100-Hz EA. (3) 100-Hz EA was very effective in suppressing NX-precipitated morphine withdrawal syndrome. This effect of EA could be prevented by intrathecal administration of nor-BNI (2.5 μg/20 μl), a κ-opioid receptor antagonist, or dynorphin A (1–13) antibodies (25 μg/20 μl) administered 10 min prior to EA. In conclusion, while the steady-state spinal dynorphin release is low in morphine-dependent rats, it can be activated by 100-Hz EA stimulation, which may be responsible for eliciting an analgesic effect and ameliorating morphine withdrawal syndrome, most probably via interacting with κ-opioid receptor at spinal level.     

Inhibitory effect of electroacupuncture (EA) on the pressor response induced by exercise stress

Abstract. We examined the effect of EA on the exercise stress-induced pressor response in healthy adult subjects of both sexes. Each subject was subjected to a bicycle exercise test using a ramp protocol once/week for three or four weeks. Subjects were asked to perform the following tests in random order: 1) a baseline exercise test without EA and 2) exercise after acupuncture at P 5–6, LI 4-L 7 and/or G 37–39 acupoints. Brachial systolic (SBP), diastolic (DBP), and mean blood pressures (MBP), heart rate (HR) and the rate-pressure product (RPP, systolic BP x HR/100) were measured every three min, while a 12 lead ECG was monitored continuously. We observed increases in MBP, SBP, HR and RPP in all 17 subjects during exercise. In 12 of the 17 subjects (71 %), EA for 30 min before exercise, either at Jianshi-Neiguan acupoints (P 5–6) or Hegu-Lique acupoints (LI 4-L 7), led to an increase in maximal workload, and reduced peak SBP, MBP and RPP responses to exercise; EA did not alter DBP or HR responses in these subjects. EA at control acupoints (Guangming-Xuanzhong acupoints, G 37–39) in five subjects did not alter the hemodynamic responses. Seven additional subjects were enrolled to study the effect of EA during a bicycle exercise test using a constant workload. The results were similar, in five of the seven subjects SBP, MBP and RPP after exercise were attenuated significantly by EA at P 5–6. We conclude that EA at specific acupoints improves exercise capacity and reduces the hemodynamic responses in approximately 70% of normal subjects.This project is supported by the DANA Foundation, the Susan-Sameuli Center for Integrative Medicine at UCI, the Larry K. Dodge Chair in Integrative Biology (JCL), and the General Clinical Research Center of UCI (5M61RR000827).     

Ovarian blood flow responses to electro-acupuncture stimulation at different frequencies and intensities in anaesthetized rats

The purpose of the present study was to investigate changes in ovarian blood flow (OBF) in response to electro-acupuncture (EA) stimulation at different frequencies and intensities in anaesthetized rats. Whether the ovarian sympathetic nerves were involved in OBF responses was elucidated by severance of the ovarian sympathetic nerves. In addition, how changes in the systemic circulation affected OBF was evaluated by continuously recording blood pressure. OBF was measured on the surface of the left ovary using laser Doppler flowmeter. Acupuncture needles with a diameter of 0.3 mm were inserted bilaterally into the abdominal and the hindlimb muscles and connected to an electrical stimulator. Two frequencies-2 Hz (low) and 80 Hz (high)-with three different intensities-1.5, 3, and 6 mA-were applied for 35 s. Both low- and high-frequency EA at 1.5 mA and high-frequency EA at 3 mA had no effect on OBF or mean arterial blood pressure (MAP). Low-frequency EA at 3 and 6 mA elicited significant increases in OBF. In contrast, high-frequency EA with an intensity of 6 mA evoked significant decreases in OBF, followed by decreases in MAP. After severance of the ovarian sympathetic nerves, the increases in the OBF responses to low-frequency EA at 3 and 6 mA were totally abolished, and the responses at 6 mA showed a tendency to decrease, probably because of concomitant decreases in MAP. The decreased OBF and MAP responses to high-frequency EA at 6 mA remained after the ovarian sympathectomy, and the difference in the responses before and after ovarian sympathectomy was nonsignificant.In conclusion, the present study showed that low-frequency EA stimulation increases OBF as a reflex response via the ovarian sympathetic nerves, whereas high-frequency EA stimulation decreases OBF as a passive response following systemic circulatory changes.     

Effects of electroacupuncture on cold allodynia in a rat model of neuropathic pain: mediation by spinal adrenergic and serotonergic receptors

The present study was performed to examine the effects of electroacupuncture (EA) on cold allodynia and its mechanisms related to the spinal adrenergic and serotonergic systems in a rat model of neuropathic pain. For the neuropathic surgery, the right superior caudal trunk was resected at the level between S1 and S2 spinal nerves innervating the tail. Two weeks after the nerve injury, EA stimulation (2 or 100 Hz) was delivered to Zusanli (ST36) for 30 min. The behavioral signs of cold allodynia were evaluated by the tail immersion test [i.e., immersing the tail in cold water (4 degrees C) and measuring the latency to an abrupt tail movement] before and after the stimulation. And then, we examined the effects of intrathecal injection of prazosin (alpha1-adrenoceptor antagonist, 30 microg), yohimbine (alpha2-adrenoceptor antagonist, 30 microg), NAN-190 (5-HT1A antagonist, 15 microg), ketanserin (5-HT2A antagonist, 30 microg), and MDL-72222 (5-HT3 antagonist, 12 microg) on the action of EA stimulation. Although both 2 Hz and 100 Hz EA significantly relieved the cold allodynia signs, 2 Hz EA induced more robust effects than 100 Hz EA. In addition, intrathecal injection of yohimbine, NAN-190, and MDL-72222, but not prazosin and ketanserin, significantly blocked the relieving effects of 2 Hz EA on cold allodynia. These results suggest that low-frequency (2 Hz) EA is more suitable for the treatment of cold allodynia than high-frequency (100 Hz) EA, and spinal alpha2-adrenergic, 5-HT1A and 5-HT3, but not alpha1-adrenergic and 5-HT2A, receptors play important roles in mediating the relieving effects of 2 Hz EA on cold allodynia in neuropathic rats.     

Long-term synaptic plasticity in the spinal dorsal horn and its modulation by electroacupuncture in rats with neuropathic pain

Our previous study has reported that electroacupuncture (EA) at low frequency of 2 Hz had greater and more prolonged analgesic effects on mechanical allodynia and thermal hyperalgesia than that EA at high frequency of 100 Hz in rats with neuropathic pain. However, how EA at different frequencies produces distinct analgesic effects on neuropathic pain is unclear. Neuronal plastic changes in spinal cord might contribute to the development and maintenance of neuropathic pain. In the present study, we investigated changes of spinal synaptic plasticity in the development of neuropathic pain and its modulation by EA in rats with neuropathic pain. Field potentials of spinal dorsal horn neurons were recorded extracellularly in sham-operated rats and in rats with spinal nerve ligation (SNL). We found for the first time that the threshold for inducing long-term potentiation (LTP) of C-fiber-evoked potentials in dorsal horn was significantly lower in SNL rats than that in sham-operated rats. The threshold for evoking the C-fiber-evoked field potentials was also significantly lower, and the amplitude of the field potentials was higher in SNL rats as compared with those in the control rats. EA at low frequency of 2 Hz applied on acupoints ST 36 and SP 6, which was effective in treatment of neuropathic pain, induced long-term depression (LTD) of the C-fiber-evoked potentials in SNL rats. This effect could be blocked by N-methyl-d-aspartic acid (NMDA) receptor antagonist MK-801 and by opioid receptor antagonist naloxone. In contrast, EA at high frequency of 100 Hz, which was not effective in treatment of neuropathic pain, induced LTP in SNL rats but LTD in sham-operated rats. Unlike the 2 Hz EA-induced LTD in SNL rats, the 100 Hz EA-induced LTD in sham-operated rats was dependent on the endogenous GABAergic and serotonergic inhibitory system. Results from our present study suggest that (1) hyperexcitability in the spinal nociceptive synaptic transmission may occur after nerve injury, which may contribute to the development of neuropathic pain; (2) EA at low or high frequency has a different effect on modulating spinal synaptic plasticities in rats with neuropathic pain. The different modulation on spinal LTD or LTP by low- or high-frequency EA may be a potential mechanism of different analgesic effects of EA on neuropathic pain. LTD of synaptic strength in the spinal dorsal horn in SNL rats may contribute to the long-lasting analgesic effects of EA at 2 Hz.     

Genome-wide association study of alcohol dependence implicates KIAA0040 on chromosome 1q

Previous studies using SAGE (the Study of Addiction: Genetics and Environment) and COGA (the Collaborative Study on the Genetics of Alcoholism) genome-wide association study (GWAS) data sets reported several risk loci for alcohol dependence (AD), which have not yet been well replicated independently or confirmed by functional studies. We combined these two data sets, now publicly available, to increase the study power, in order to identify replicable, functional, and significant risk regions for AD. A total of 4116 subjects (1409 European-American (EA) cases with AD, 1518 EA controls, 681 African-American (AA) cases, and 508 AA controls) underwent association analysis. An additional 443 subjects underwent expression quantitative trait locus (eQTL) analysis. Genome-wide association analysis was performed in EAs to identify significant risk genes. All available markers in the genome-wide significant risk genes were tested in AAs for associations with AD, and in six HapMap populations and two European samples for associations with gene expression levels. We identified a unique genome-wide significant gene--KIAA0040--that was enriched with many replicable risk SNPs for AD, all of which had significant cis-acting regulatory effects. The distributions of -log(p) values for SNP-disease and SNP-expression associations for all markers in the TNN-KIAA0040 region were consistent across EAs, AAs, and five HapMap populations (0.369 ≤ r ≤ 0.824; 2.8 × 10?? ≤ p ≤ 0.032). The most significant SNPs in these populations were in high LD, concentrating in KIAA0040. Finally, expression of KIAA0040 was significantly (1.2 × 10?11 ≤ p ≤1 .5 × 10??) associated with the expression of numerous genes in the neurotransmitter systems or metabolic pathways previously associated with AD. We concluded that KIAA0040 might harbor a causal variant for AD and thus might directly contribute to risk for this disorder. KIAA0040 might also contribute to the risk of AD via neurotransmitter systems or metabolic pathways that have previously been implicated in the pathophysiology of AD. Alternatively, KIAA0040 might regulate the risk via some interactions with flanking genes TNN and TNR. TNN is involved in neurite outgrowth and cell migration in hippocampal explants, and TNR is an extracellular matrix protein expressed primarily in the central nervous system.     

Electroacupuncture induces c-Fos expression in the rostral ventrolateral medulla and periaqueductal gray in cats: relation to opioid containing neurons

Our previous studies have shown that electroacupuncture (EA) at the Neiguan-Jianshi (P5-P6) acupoints inhibits sympathetic outflow and attenuates excitatory visceral cardiovascular reflexes through enkephalin- or beta-endorphin-related opioid receptors in the rostral ventrolateral medulla (rVLM). It is not known whether EA at these acupoints activates neurons containing enkephalin or beta-endorphin in the rVLM as well as in the periaqueductal gray (PAG) that are involved in EA-mediated central neural regulation of sympathetic activity. The present study evaluated activated neurons in the rVLM and PAG by detecting c-Fos immunoreactivity, and identified the relationship between c-Fos nuclei and neuronal structures containing enkephalin or beta-endorphin in these regions. To enhance the detection of cell bodies containing enkephalin or beta-endorphin, colchicine (90-100 microg/kg) was injected into the subarachnoid space in anesthetized cats 28-30 h prior to EA or the sham-operated control for EA. Following bilateral barodenervation and cervical vagotomy, EA (1-4 mA, 2 Hz, 0.5 ms) was performed at the P5-P6 acupoints (overlying median nerve; n=7) for 30 min. Identical procedures, with the exception of electrical stimulation, were carried out in five control animals. EA decreased blood pressure (BP) in four of seven cats (5-15 mm Hg) while the sham procedure for EA produced no responses. Perikarya containing enkephalin were found in the rVLM and rarely in the PAG, while no cell bodies labeled with beta-endorphin were identified in either region. Compared to animals in the control group, more c-Fos immunoreactivity, located principally in close proximity to fibers containing enkephalin or beta-endorphin, was observed in the rVLM and ventrolateral PAG (vlPAG) in EA-treated cats. Moreover, neurons double-labeled with c-Fos and enkephalin in the rVLM were significantly increased in cats following EA stimulation (P<0.05). These data indicate that EA at the P5-P6 acupoints activates neurons in the rVLM and vlPAG. These activated neurons contain enkephalin in the rVLM, and most likely interact with nerve fibers containing enkephalin or beta-endorphin in both the rVLM and vlPAG. The results from this study provide the first anatomical evidence showing that EA at the P5-P6 acupoints has the potential to influence neuronal structures (perikarya, axons and/or dendrites) containing enkephalin or beta-endorphin in specific regions of the brain stem. These neurons likely form the substrate for EA's influence on sympathoexcitatory cardiovascular reflexes.     

Electroacupuncture attenuates morphine withdrawal signs and c-Fos expression in the central nucleus of the amygdala in freely moving rats

Experimental efforts for understanding the mechanisms of electroacupuncture (EA) for opiate addiction are partially hampered by restraint stress. In unrestrained animals, it is difficult to perform EA stimulation at acupuncture points frequently selected on the four limbs. The present study was performed to evaluate the effect of EA at the acupuncture point Shen-Shu (BL.23) on morphine withdrawal signs and c-Fos expression of the amygdala in freely moving rats or restrained rats. We applied immunohistochemistry to detect c-Fos-positive nuclei. Corticosterone levels and behavioral responses were measured during EA stimulation. The needles were bilaterally inserted and fixed at BL.23, and 100-Hz electric stimulation was conducted 30 min before naloxone-precipitated withdrawal. In both freely moving rats and restrained rats, EA significantly reduced the signs of morphine withdrawal. Notably, EA stimulation in freely moving rats attenuated c-Fos expression in the central nucleus of the amygdala while EA in restrained animals increased this response. In addition, the restrained rats emitted greater levels of vocalization and facial expression than freely moving rats during EA stimulation. Corticosterone levels were also significantly higher in restrained animals after EA stimulation. The new EA paradigm demonstrated in the present study might help the analysis of certain physiological responses induced by EA that would otherwise have been hindered by restraint stress.     

Protective effects of electroacupuncture on cardiac function in rats subjected to thoracic surgery trauma

The present study investigates the protective effects of electroacupuncture (EA) application on cardiac function, while simultaneously exploring the underlying neurobiological mechanisms, in rats that have experienced thoracic surgery-induced stress. Mean arterial and left intraventricular pressures were monitored as indicators of cardiac function. Meanwhile, the immunohistochemistry for c-Fos protein expression and electrophysiology in vitro in brain nuclei, known to regulate cardiac function, provide insights into the effects of EA on the central nervous system. The results show that cardiac function was dramatically suppressed with thoracic surgery trauma, the expression levels of c-Fos in the paraventricular nucleus (PVN) and the rostral ventrolateral medulla (RVLM) significantly increased, the rheobase intensity of the intracellular current injection needed to initiate the action potential decreased, membrane resistance in the PVN neurons significantly increased, and the inductivity of the postsynaptic potentials in the PVN neurons of the surgery-treated rats significantly decreased. EA application at the Neiguan acupoints (PC6) attenuated the decreases in almost all investigated functional parameters of the heart. EA significantly decreased the number of Fos-immunoreactive neurons in the PVN and RVLM, significantly decreased the Max L. slope of the PVN neurons, and increased the inductivity of the postsynaptic potentials in the PVN neurons of the surgery-treated rats. These data indicate the protective effects of EA application on cardiac function in rats that have experienced surgery-induced stress and show that EA application at the Neiguan acupoints may produce its protective effects through the neurons in the PVN and the RVLM.     

Peripheral mechanical loading and the mechanism of the tremor of chronic alcoholism.

The tremor of chronic alcoholism, although clinically similar to essential tremor, has been considered a distinct syndrome. Its underlying mechanism was analyzed in five patients (none in the acute stages of alcohol withdrawal) hospitalized in an alcohol detoxification program. All five patients performed tracking tasks in which they pursued a linearly moving "target" light with a response light that they controlled by flexion-extension activity of the wrist. Stationary and dynamic targets were used with both isometric and unconstrained wrist mechanical interfaces. Frequency, torque, and displacement tremor characteristics were examined under varying inertial loading or isometric voluntary torque conditions. Two simultaneous tremor components were present in all patients: a prominent 4- to 7-Hz low-frequency peak and a smaller-amplitude 9.4- to 9.6-Hz high-frequency peak. As the inertia of the hand was augmented during unconstrained tasks, the low-frequency peak decreased, while the high-frequency peak was unaffected. As required voluntary effort was increased during isometric testing, the amplitude of the low-frequency peak increased. These findings suggest that the low-frequency peak represents the significant pathologic component of the tremor of chronic alcoholism and that it has a biomechanical reflex mechanism similar to that of the lower-amplitude normal physiologic tremor.