Capsaicin-sensitive afferentation represents an indifferent defensive pathway from eradication in patients with H.pylori gastritis

AIM:To study the role of capsaicin-sensitive afferent nerves in Helicobacter pylori (H.pylori) positive chronic gastritis before and after eradication.METHODS:Gastric biopsy samples were obtained from corpus and antrum mucosa of 20 healthy human subjects and 18 patients with H.pylori positive chronic gastritis (n=18) before and after eradication.Tradi-tional gastric mucosal histology (and Warthin-Starry silver impregnation) and special histochemical examina-tions were carried out.Immunohistochemistry for cap-saicin receptor (TRVP1),calcitonin gene-related peptide (CGRP) and substance P (SP) were carried out by the labeled polymer immunohistological method (Lab VisionCo.,USA) using polyclonal rabbit and rat monoclonal antibodies (Abcam Ltd.,UK).RESULTS:Eradication treatment was successful in 16 patients (89%).Seven patients (7/18,39%) re-mained with moderate complaints,meanwhile 11 pa-tients (11/28,61%) had no complaints.At histological evaluation,normal gastric mucosa was detected in 4 patients after eradication treatment (4/18,22%),and moderate chronic gastritis could be seen in 14 (14/18,78%) patients.Positive immuno-staining for capsaicin receptor was seen in 35% (7/20) of controls,89% (16/18,P < 0.001) in patients before and 72% (13/18,P < 0.03) after eradication.CGRP was positive in 40% (8/20) of controls,and in 100% (18/18,P < 0.001) of patients before and in 100% (18/18,P < 0.001) after eradication.The immune-staining of gastric mucosa for substance-P was positive in 25% (5/20) of healthy con-trols,and in 5.5% (3/18,P > 0.05) of patients before and in 0% of patients (0/18,P > 0.05) after H.pylori eradication.CONCLUSION:Distibution of TRVP1 and CGRP is altered during the development of H.pylori positive chronic gastritis.The immune-staining for TRVP1,CGRP and SP rwemained unchanged before and after H.py-lori eradication treatment.The capsaicin-sensitive affer-entation is an independent from the eradication treat-ment.The 6 wk time period might not be enough time for the restituion of chronic H.pylori positive chronic gastritis.The H.pylori infection might not represent the main pathological factor in the development of chronic

Interplay between inflammation,immune system and neuronal pathways:Effect on gastrointestinal motility

Sepsis is a systemic inflammatory response representing the leading cause of death in critically ill patients,mostly due to multiple organ failure.The gastrointestinal tract plays a pivotal role in the pathogenesis of sepsisinduced multiple organ failure through intestinal barrier dysfunction,bacterial translocation and ileus.In this review we address the role of the gastrointestinal tract,the mediators,cell types and transduction pathways involved,based on experimental data obtained from models of inflammation-induced ileus and (preliminary) clinical data.The complex interplay within the gastrointestinal wall between mast cells,residential macrophages and glial cells on the one hand,and neurons and smooth muscle cells on the other hand,involves intracellular signaling pathways,Toll-like receptors and a plethora of neuroactive substances such as nitric oxide,prostaglandins,cytokines,chemokines,growth factors,tryptases and hormones.Multidirectional signaling between the different components in the gastrointestinal wall,the spinal cord and central nervous system impacts inflammation and its consequences.We propose that novel therapeutic strategies should target inflammation on the one hand and gastrointestinal motility,gas-trointestinal sensitivity and even pain signaling on the other hand,for instance by impeding afferent neuronal signaling,by activation of the vagal anti-inflammatory pathway or by the use of pharmacological agents such as ghrelin and ghrelin agonists or drugs interfering with the endocannabinoid system.

Neuromechanism of acupuncture regulating gastrointestinal motility

Acupuncture has been used in China for thousands of years and has become more widely accepted by doctors and patients around the world. A large number of clinical studies and animal experiments have confirmed that acupuncture has a benign adjustment effect on gastrointestinal(GI) movement;however, the mechanism of this effect is unclear, especially in terms of neural mechanisms, and there are still many areas that require further exploration. This article reviews the recent data on the neural mechanism of acupuncture on GI movements. We summarize the neural mechanism of acupuncture on GI movement from four aspects: acupuncture signal transmission, the sympathetic and parasympathetic nervous system, the enteric nervous system, and the central nervous system.

Neuroanatomy of lower gastrointestinal pain disorders

Chronic abdominal pain accompanying intestinal inflammation emerges from the hyperresponsiveness of neuronal,immune and endocrine signaling pathways within the intestines,the peripheral and the central nervous system.In this article we review how the sensory nerve information from the healthy and the hypersensitive bowel is encoded and conveyed to the brain.The gut milieu is continuously monitored by intrinsic enteric afferents,and an extrinsic nervous network comprising vagal,pelvic and splanchnic afferents.The extrinsic afferents convey gut stimuli to second order neurons within the superficial spinal cord layers.These neurons cross the white commissure and ascend in the anterolateral quadrant and in the ipsilateral dorsal column of the dorsal horn to higher brain centers,mostly subserving regulatory functions.Within the supraspinal regions and the brainstem,pathways descend to modulate the sensory input.Because of this multiple level control,only a small proportion of gut signals actually reaches the level of consciousness to induce sensation or pain.In inflammatory bowel disease(IBD)and irritable bowel syndrome(IBS)patients,however,long-term neuroplastic changes have occurred in the brain-gut axis which results in chronic abdominal pain.This sensitization may be driven on the one hand by peripheral mechanisms within the intestinal wall which encompasses an interplay between immunocytes,enterochromaffin cells,resident macrophages,neurons and smooth muscles.On the other hand,neuronal synaptic changes along with increased neurotransmitter release in the spinal cord and brain leads to a state of central wind-up.Also life factors such as but not limited to inflammation and stress contribute to hypersensitivity.All together,the degree to which each of these mechanisms contribute to hypersensitivity in IBD and IBS might be diseaseand even patient-dependent.Mapping of sensitization throughout animal and human studies may significantly improve our understanding of sensitization in IBD and IBS.On the long run,this knowledge can be put forward in potential therapeutic targets for abdominal pain in these conditions.

Management of afferent loop obstruction: Reoperation or endoscopic and percutaneous interventions?

Afferent loop obstruction is a purely mechanical complication that infrequently occurs following construction of a gastrojejunostomy. The operations most commonly associated with this complication are gastrectomy with Billroth Ⅱ or Roux-en-Y reconstruction, and pancreaticoduodenectomy with conventional loop or Roux-en-Y reconstruction. Etiology of afferent loop obstruction includes:(1) entrapment, compression and kinking by postoperative adhesions;(2) internal herniation, volvulus and intussusception;(3) stenosis due to ulceration at the gastrojejunostomy site and radiation enteritis of the afferent loop;(4) cancer recurrence; and(5) enteroliths, bezoars and foreign bodies. Acute afferent loop obstruction is associated with complete obstruction of the afferent loop and represents a surgical emergency, whereas chronic afferent loop obstruction is associated with partial obstruction. Abdominal multiple detector computed tomography is the diagnostic study of choice. CT appearance of the obstructed afferent loop consists of a C-shaped, fluidfilled tubular mass located in the midline between the abdominal aorta and the superior mesenteric artery with valvulae conniventes projecting into the lumen. The cornerstone of treatment is surgery. Surgery includes:(1) adhesiolysis and reconstruction for benign causes; and(2) by-pass or excision and reconstruction for malignant causes. However, endoscopic enteral stenting, transhepatic percutaneous enteral stenting and direct percutaneous tube enterostomy have the principal role in management of malignant and radiation-induced obstruction. Nevertheless, considerable limitations exist as a former Roux-en-Y reconstruction limits endoscopic access to the afferent loop and percutaneous approaches for enteral stenting and tube enterostomy have only been reported in the literature as isolated cases.

Gastro-protective action of lafutidine mediated by capsaicin-sensitive afferent neurons without interaction with TRPV1 and involvement of endogenous prostaglandins

AIM： Lafutidine, a histamine H2 receptor antagonist, exhibits gastro-protective action mediated by capsaicinsensitive afferent neurons （CSN）. We compared the effect between lafutidine and capsaicin, with respect to the interaction with endogenous prostaglandins （PG）, nitric oxide （NO） and the afferent neurons, including transient receptor potential vanilloid subtype 1 （TRPV1）. METHODS： Male SD rats and C57BL/6 mice, both wildtype and prostacyclin IP receptor knockout animals, were used after 18 h of fasting. Gastric lesions were induced by the po administration of HCl/ethanol （60% in 150 mmol/L HCl） in a volume of 1 mL for rats or 0.3 mL for mice. RESULTS： Both lafutidine and capsaicin （1-10 mg/kg, po） afforded dose-dependent protection against HCI/ ethanol in rats and mice. The effects were attenuated by both the ablation of CSN and pretreatment with NG-nitro- L-arginine methyl ester, yet only the effect of capsaicin was mitigated by prior administration of capsazepine, the TRPV1 antagonist, as well as indomethacin. Lafutidine protected the stomach against HCl/ethanol in IP receptor knockout mice, similar to wild-type animals, while capsaicin failed to afford protection in the animals lacking IP receptors. Neither of these agents affected the mucosal PGE2 or 6-keto PGF1α contents in rat stomachs. Capsaicin evoked an increase in [Ca^2＋]i in rat TRPV1-transfected HEK293 cells while lafutidine did not. CONCLUSION： These results suggest that although both lafutidine and capsaicin exhibit gastro-protective action mediated by CSN, the mode of their effects differs regarding the dependency on endogenous PGs/IP receptors and TRPV1. It is assumed that lafutidine interacts with CSN at yet unidentified sites other than TRPV1.

The existence of propagated sensation along the meridian proved by neuroelectrophysiology

Propagated sensation along the meridian can occur when acupoints are stimulated by acupuncture or electrical impulses. In this study, participants with notable propagated sensation along the me- ridian were given electro-acupuncture at the Jianyu （LI15） acupoint of the large intestine meridian. When participants stated that the sensation reached the back of their hand, reguJar nervous system action discharge was examined using a physiological recording electrode placed on the superficial branch of the radial nerve. The topographical maps of brain-evoked potential in the primary cortical somatosensory area were also detected. When Guangming （GB37） acupoint in the lower limb and Hegu （LI4） acupoint in the upper limb were stimulated, subjects without propagated sensation along the meridian exhibited a high potential reaction in the corresponding area of the brain cortical somatosensory area. For subjects with a notable propagated sensation along the meridian, the re- action area was larger and extended into the face representative area. These electrophysiological measures directly prove the existence of propagated sensation along the meridian, and the periph- eral stimulated site is consistent with the corresponding primary cortical somatosensory area, which presents a high potential reaction.

Hyperpolarization-activated cyclic nucleotide-gated cation channel subtypes differentially modulate the excitability of murine small intestinal afferents

AIM： To assess the role of hyperpolarization-activated cyclic nucleotide-gated cation （HCN） channels in regu- lating the excitability of vagal and spinal gut afferents. METHODS： The mechanosensory response of mesen- teric afferent activity was measured in an ex vivo murine jejunum preparation. HCN channel activity was recorded through voltage and current clamp in acutely dissoci- ated dorsal root ganglia （DRG） and nodose ganglia （NG） neurons retrogradely labeled from the small intestine through injection of a fluorescent marker （DiI）. The isoforms of HCN channels expressed in DRG and NG neurons were examined by immunohistochemistry. RESULTS： Ramp distension of the small intestine evok- ed biphasic increases in the afferent nerve activity, re- flecting the activation of low- and high-threshold fibers.HCN blocker CsCl （5 mmol/L） preferentially inhibited the responses of low-threshold fibers to distension and showed no significant effects on the high-threshold re- sponses. The effect of CsCI was mimicked by the more selective HCN blocker ZD7288 （10 ~mol/L）. In 71.4% of DiI labeled DRG neurons （/7 = 20） and 90.9% of DiI labeled NG neurons （n = 10）, an inward current （Ih current） was evoked by hyperpolarization pulses which was fully eliminated by extracellular CsCI. In neurons expressing Ih current, a typical ＂sag＂ was observed upon injection of hyperpolarizing current pulses in cur- rent-clamp recordings. CsCI abolished the sag entirely. In some DiI labeled DRG neurons, the Ih current was potentiated by 8-Br-cAMP, which had no effect on the Ih current of DiI labeled NG neurons. Immunohistochem- istry revealed differential expression of HCN isoforms in vagal and spinal afferents, and HCN2 and HCN3 seemed to be the dominant isoform in DRG and NG, respec- tively.CONCLUSION： HCNs differentially regulate the excit- ability of vagal and spinal afferent of murine small in- testine.

Exposure to blast shock waves via the ear canal induces deficits in vestibular afferent function in rats

The ears are air-filled structures that are directly impacted during blast exposure.In addition to hearing loss and tinnitus,blast victims often complain of vertigo,dizziness and unsteady posture,suggesting that blast exposure induces damage to the vestibular end organs in the inner ear.However,the underlying mechanisms remain to be elucidated.In this report,single vestibular afferent activity and the vestibuloocular reflex(VOR)were investigated before and after exposure to blast shock waves(~20 PSI)delivered into the left external ear canals of anesthetized rats.Single vestibular afferent activity was recorded from the superior branch of the left vestibular nerves of the blast-treated and control rats one day after blast exposure.Blast exposure reduced the spontaneous discharge rates of the otolith and canal afferents.Blast exposure also reduced the sensitivity of irregular canal afferents to sinusoidal head rotation at 0.5e2Hz.Blast exposure,however,resulted in few changes in the VOR responses to sinusoidal head rotation and translation.To the best of our knowledge,this is the first study that reports blast exposure-induced damage to vestibular afferents in an animal model.These results provide insights that may be helpful in developing biomarkers for early diagnosis of blast-induced vestibular deficits in military and civilian populations.

Management of afferent loop obstruction from recurrent metastatic pancreatic cancer using a venting gastrojejunostomy

Pancreatic cancer is an aggressive malignancy poten-tially curable with surgical intervention. Following pan-creaticoduodenectomy for suspected pancreatic head malignancy, patients have a high risk for both immedi-ate and delayed problems due to surgical complica-tions and recurrent disease. We report here a patient with pancreatic cancer treated with pancreaticoduode-nectomy who developed recurrent disease resulting in obstruction of the afferent limb. The patient developed biliary obstruction and cholangitis at presentation. Her biliary tree failed to dilate which precluded safe percu-taneous biliary decompression. During surgical explo-ration, she was found to have a dilated afferent limb at the level of the transverse mesocolon. The patient underwent decompression of the afferent limb as well as the biliary tree using a venting gastrojejunostomy to the blind loop. This represents a novel surgical ap-proach for management of this complicated and diffi-cult problem.

Expression and effect of sodium-potassium-chloride cotransporter on dorsal root ganglion neurons in a rat model of chronic constriction injury

Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain.We investigated whether the increase of NKCC1 and KCC2 is associated with peripheral pain transmission in dorsal root ganglion neurons.To this aim,rats with persistent hyperalgesia were randomly divided into four groups.Rats in the control group received no treatment,and the rat sciatic nerve was only exposed in the sham group.Rats in the chronic constriction injury group were established into chronic constriction injury models by ligating sciatic nerve and rats were given bumetanide,an inhibitor of NKCC1,based on chronic constriction injury modeling in the chronic constriction injury + bumetanide group.In the experiment measuring thermal withdrawal latency,bumetanide (15 mg/kg) was intravenously administered.In the patch clamp experiment,bumetanide (10 μg/μL) and acutely isolated dorsal root ganglion neurons (on day 14) were incubated for 1 hour,or bumetanide (5 μg/μL) was intrathecally injected.The Hargreaves test was conducted to detect changes in thermal hyperalgesia in rats.We found that the thermal withdrawal latency of rats was significantly decreased on days 7,14,and 21 after model establishment.After intravenous injection of bumetanide,the reduction in thermal retraction latency caused by model establishment was significantly inhibited.Immunohistochemistry and western blot assay results revealed that the immune response and protein expression of NKCC1 in dorsal root ganglion neurons of the chronic constriction injury group increased significantly on days 7,14,and 21 after model establishment.No immune response or protein expression of KCC2 was observed in dorsal root ganglion neurons before and after model establishment.The Cl^– (chloride ion) fluorescent probe technique was used to evaluate the change of Cl^– concentration in dorsal root ganglion neurons of chronic constriction injury model rats.We found that the relative optical density of N-(ethoxycarbonylmethyl)-6-methoxyquinolinium bromide (a Cl^– fluorescent probe whose fluorescence Cenintensity decreases as Cl– concentration increases) in the dorsal root ganglion neurons of the chronic constriction injury group was significantly decreased on days 7 and 14 after model establishment.The whole-cell patch clamp technique revealed that the resting potential and action potential frequency of dorsal root ganglion neurons increased,and the threshold and rheobase of action potentials decreased in the chronic constriction injury group on day 14 after model establishment.After bumetanide administration,the above indicators were significantly suppressed.These results confirm that CCI can induce abnormal overexpression of NKCC1,thereby increasing the Cl^– concentration in dorsal root ganglion neurons;this then enhances the excitability of dorsal root ganglion neurons and ultimately promotes hyperalgesia and allodynia.In addition,bumetanide can achieve analgesic effects.All experiments were approved by the Institutional Ethics Review Board at the First Affiliated Hospital,College of Medicine,Shihezi University,China on February 22,2017 (approval No.A2017-169-01).

Axonotmesis-evoked plantar vasodilatation as a novel assessment of C-fiber afferent function after sciatic nerve injury in rats

Quantitative assessment of the recovery of nerve function, especially sensory and autonomic nerve function, remains a challenge in the field of nerve regeneration research. We previously found that neural control of vasomotor activity could be potentially harnessed to evaluate nerve function. In the present study, five different models of left sciatic nerve injury in rats were established: nerve crush injury, nerve transection/ suturing, nerve defect/autografting, nerve defect/conduit repair, and nerve defect/non-regeneration. Laser Doppler perfusion imaging was used to analyze blood perfusion of the hind feet. The toe pinch test and walking track analysis were used to assess sensory and motor functions of the rat hind limb, respectively. Transmission electron microscopy was used to observe the density of unmyelinated axons in the injured sciatic nerve. Our results showed that axonotmesis-evoked vasodilatation in the foot 6 months after nerve injury/repair recovered to normal levels in the nerve crush injury group and partially in the other three repair groups;whereas the nerve defect/non-regeneration group exhibited no recovery in vasodilatation. Furthermore, the recovery index of axonotmesis-evoked vasodilatation was positively correlated with toe pinch reflex scores and the density of unmyelinated nerve fibers in the regenerated nerve. As C-fiber afferents are predominantly responsible for dilatation of the superficial vasculature in the glabrous skin in rats, the present findings indicate that axonotmesis-evoked vasodilatation can be used as a novel way to assess C-afferent function recovery after peripheral nerve injury. This study was approved by the Ethics Committee for Laboratory Animals of Nantong University of China (approval No. 20130410-006) on April 10, 2013.

Biliary stone causing afferent loop syndrome and pancreatitis

We report the case of an 84-year-old female who had a partial gastrectomy with Billroth-Ⅱ anastomosis 24 years ago for a benign peptic ulcer who now presented an acute pancreatitis secondary to an afferent loop syndrome. The syndrome was caused by a gallstone that migrated through a cholecystoenteric fistula. This is the first description in the literature of a biliary stone causing afferent loop syndrome.

Reactive oxygen species in paraventricular nucleus involved in cardiac sympathetic afferent reflex in rats

Objective： The present study was designed to determine if reactive oxygen species （ROS） in the paraventricular nucleus （PVN） were involved in modulating cardiac sympathetic afferent reflex （CSAR） in anesthetized rats. Methods： Malondialdehyde （MDA）, the end product of lipid peroxidation, in the PVN, was determined by thiobarbituric acid （TBA） spectrometric method. Renal sympathetic nerve activity （RSNA） and arterial pressure were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the response of the RSNA evoked by epicardial application of bradykinin （BK, 0.4 9g）. Results： The MDA in the PVN was significantly increased after epicardial application of BK compared with control （2.0 ±0.3 vs 0.8 ±0.1 nmol/mg protein, P 〈 0.01）. Microinjection of a superoxide anion scavenger, tiron （20 nmol） into the PVN significantly inhibited the CSAR evoked by BK （12.3±1.9 vs4.2± 1.2%, P 〈0.01） and decreased MDA level （1.9±0.3 vs 0.6 ±0.1 nmol/mg protein, P 〈0.01） compared with control. Conclusion： The ROS in the PVN is involved in modulating the CSAR in rats.

Expression of gamma-aminobutyric acid type A receptor α_2 subunit in the dorsal root ganglion of rats with sciatic nerve injury

The γ-aminobutyric acid neurotransmitter in the spinal cord dorsal horn plays an important role in pain modulation through primary afferent-mediated presynaptic inhibition. The weakening of γ-aminobutyric acid-mediated presynaptic inhibition may be an important cause of neuropathic pain. γ-aminobutyric acid-mediated presynaptic inhibition is related to the current strength of γ-aminobutyric acid A receptor activation. In view of this, the whole-cell patch-clamp technique was used here to record the change in muscimol activated current of dorsal root ganglion neurons in a chronic constriction injury model. Results found that damage in rat dorsal root ganglion neurons following application of muscimol caused concentration-dependent activation of current, and compared with the sham group, its current strength and γ-aminobutyric acid A receptor protein expression decreased. Immunofluorescence revealed that γ-aminobutyric acid type A receptor α2 subunit protein expression decreased and was most obvious at 12 and 15 days after modeling. Our experimental findings confirmed that the y-aminobutyric acid type A receptor α2 subunit in the chronic constriction injury model rat dorsal root ganglion was downregulated, which may be one of the reasons for the reduction of injury in dorsal root ganglion neurons following muscimol-activated currents.

PLASMA EXTRAVASATION IN THE VISCERAL ORGANS CAUSED BY ELECTRICAL STIMULATION OF ACUPOINT "ZUSANLI" IN RATS

Objective To investigate the plasma extravasation of visceral organs caused by electrical stimulation of acupoint under the dorsal root reflex and axon reflex conditions. Methods By the means of measuring the content of Evans blue, this study investigated the plasma extravasation of visceral organs induced by electrical stimulation of acupoint 'Zusanli'(ST 36).Results The Evans blue content in the visceral organs such as liver, spleen, pancreas and the whole gastrointestinal tract in rats increased significantly after electrical stimulation of acupoint 'Zusanli' compared with that of the control group (P<0.01). The Evans blue extravasation in the above visceral organs was blocked by pre-treatment of capsaicin (66 mmol·L -1, 50 μL) into the acupoint. Conclusion The neurogenic inflammation of the visceral organs evoked by electrical stimulation of acupoint was mediated by the capsaicin-sensitive afferent fibers through the dorsal root reflex and axon reflex. It is a new method to study the correlation of meridian-viscera.

SH2-B beta upregulates the expression of interleukin-1 beta in lung and visceral primary afferent neurons in asthmatic mice

A previous study by our research group showed that nerve growth factor is involved in the onset of asthma through regulating SH2-Bβ expression in the lung and visceral primary afferent neurons of asthmatic mice. This study sought to assess the expression level of interleukin-1β in primary afferent neurons in C7-T5 spinal ganglia, spinal cord and lung in asthmatic mice after blockage of SH2-Bβ. The levels of interleukin-1β protein in primary afferent neurons in the C7-T5 spinal ganglia and lung were decreased, and interleukin-1β mRNA expression also down-regulated in the spinal cord, medulla oblongata and lung tissue after blockage of SH2-Bβ. Our findings indicate that SH2-Bβ can upregulate the expression of interleukin-1β in C7-T5 spinal ganglia, spinal cord and lung of asthmatic mice.

A paracrine role for white thermogenic adipocytes in innervation: an evidence-based hypothesis

White adipose tissue(WAT) stores energy and also plays an important endocrine role in producing adipokines for communication with the peripheral and central nervous system. WAT consists of the major lipogenic unilocular adipocytes and the minor populations of beige and brite multilocular adipocytes. These multilocular adipocytes express thermogenic genes and have phenotypic similarity with thermogenic brown adipose tissue. According to a current paradigm, multilocular adipocytes have a thermogenic function in WAT. In this mini review, we discuss data revealing heterogeneity among multilocular cell subsets in WAT and their functions beyond thermogenesis. We propose a hypothetical neuroendocrine role for multilocular adipocytes subsets in the formation of adaptive sensory-sympathetic circuits between the central nervous system and adipose tissue, which activate lipolysis and thermogenesis in WAT in high energy demand situations.

Cortical and spinal evoked potential response to electrical stimulation in human rectum

AIM: To study a novel technique to record spinal and cortical evoked potentials (EPs) simultaneously in response to electrical stimulation in the human rectum. METHODS: Eight male and nine female healthy volunteers participated. Stimulating electrodes were attached to the rectal mucosa at 15 cm and 12 cm above the dentate line. Recording skin electrodes were positioned over vertebrae L4 through S2. The electrical stimulus was a square wave of 0.2 ms duration and the intensity of the stimulus varied between 0 and 100 mA. EP responses were recorded using a Nicolet Viking IV programmable signal conditioner.RESULTS: Simultaneous recording of cortical and spinal EPs was obtained in > 80% of the trials. The EP responses increased with the intensity of the electrical stimulation, were reproducible overtime, and were blocked by application of Lidocaine jelly at the site of stimulation. The morphology (N1/P1), mean ± SD for latency (spinal N1, 4.6 ± 0.4 ms; P1, 6.8 ± 0.5 ms; cortical N1, 136.1 ± 4.2 ms; P1, 233.6 ± 12.8 ms) and amplitude (N1/P1, spinal, 38 ± 7 μV; cortical 19 ± 3 μV) data for the EP responses were consistent with those in the published literature. Reliable and reproducible EP recordings were obtained with the attachment of the electrodes to the rectal mucosa at predetermined locations between 16 and 8 cm above the anal verge, and the distance between the attachment sites of the electrodes (the optimal distance being approximately 3.0 cm between the two electrodes). CONCLUSION: This technique can be used to assess potential abnormalities in primary afferent neural pathways innervating the rectum in several neurodegenerative and functional pain disorders.

THE CORRELATION OF CENTRAL AFFERENT OF ACUPOINTS QUANLIAO(SI 18) AND SHIBAI(ST 2): TRANSGANGLIONIC DEGENERATIVE METHOD STUDY

Using transganglionic degenerative methed, we investigated the primary afferentinformation of acupoints of Quanliao (SI 18) and Shibai(ST 2). The results showed that the largeamounts of degenerative fibers could be found bilaterally in trigeminal spinal nucleus and its tract,trigeminal principal sensory nucleus, trigeminal mesencephalic nucleus and some degenerations couldbe observed ipsilaterally in solitary tract and its nucleus, medullary lateral reticular nucleus, giganto-cellular reticular nucleus and nucleus raphe magnus following transection of infraorbital nerve. A verymoderate degenerative fibers could be identifed in ipsilateral accessory spinal nucleus and spinal reticu-lar nucleus. A few degenerative fibers were seen on the contralateral magnocellular part of caudatepart of trigeminal spinal nucleus by passing through the posterior commissure of canalis centralis.These results suggest that the primary information of acupoints of Quanliao and Shibai could be trans-mittered into the above