Auerbach plexus structure with NADH histochemistry in a line of obese rats: effects of dietary restriction

This report aims to study architectural Auerbach plexus structure with NADH histochemistry (nicotinamide adenine dinucleotide, reduced form), along ages and their modifications with restricted diet in obese beta line rats. Experimental groups were: 1) After weaning, male rats were fed ad libitum (ALD) with standard rat chow. Autopsies were done at 2, 4, 8, 12, and 18 months old. 2) After weaning, one group was fed ad libitum, another group of rats were maintained on a restricted diet (RD). Autopsy was performed at 8 months of age. 3) After weaning, male rats were fed ad libitum (ALD) with standard rat chow. At 60 days old one group was continued with standard rat chow. Another group was fed with a restricted diet (RD). Autopsy was performed at 120 days old. After autopsy, segments of small intestine, proximal and distal colon were processed for NADH histochemistry. 1) At 2 months of age some empty spaces ("neuronal ghosts") were seen between neurons. Later on partial to total disruption of reticular structures was seen along ages. 2) In RD rats of 8 months of age, a mesh-like structure similar to normal control rats was observed. In ALD rats, partial to total disruption of mesh-like structures was seen. 3) In RD rats of 4 months of age, disruption intermingled with normal mesh-like zones was seen, more severe in ALD rats. Changes in Auerbach plexus structure (disruption of mesh-like appearance) in this line of rats were quite different from normal control rats suggesting dismetabolism effects. Dietary restriction delayed alterations in Auerbach plexus structures in obese rats.     

Enteric nerves in diabetic rats: increase in vasoactive intestinal polypeptide but not substance P

The distribution of vasoactive intestinal polypeptide (VIP) and substance P-like immunoreactivities was studied by immunohistochemistry in the myenteric plexus and circular muscle layer of the ileum and proximal colon of rats 8 wk after induction of diabetes with streptozotocin. A consistent increase was observed in fluorescence intensity of VIP-like immunoreactivity in the nerve fibers, and intensely stained cell bodies were significantly more frequent in the myenteric plexus of the ileum (p less than 0.001) from diabetic animals. Some varicosities of VIP-like immunoreactive fibers in the myenteric plexus appeared to be enlarged. Vasoactive intestinal polypeptide-like immunoreactivity was increased and VIP-like immunoreactive nerves appeared thicker in the circular muscle layer of both diabetic ileum and proximal colon. The VIP levels were measured biochemically in tissue consisting of the smooth muscle layers and myenteric plexus. A significant increase in the VIP content per centimeter of intestine was found in both the ileum (p less than and proximal colon (p less than 0.01) from diabetic rats. In contrast, no apparent change in substance P innervation was observed immunohistochemically in the myenteric plexus and circular muscle layer of either diabetic ileum or proximal colon when compared with controls. The results are discussed in relation to the symptoms of autonomic neuropathy of the gut in diabetes.     

Immunochemical localization of aminopeptidase M in the alimentary tract of the guinea pig and rat.

Aminopeptidase M (APM) was localized in the kidney and alimentary tract of guinea pigs and rats by indirect immunohistochemistry. APM was detected in the brush border of the epithelium of the proximal convoluted tubule of the kidney and of the small intestine, and it was localized to cells scattered throughout lymphoid tissue in the small intestine and colon. The gastric mucosa was unstained. APM was localized to numerous fibers supplying the myenteric plexus of the stomach, small intestine, and colon. The submucosal plexus was sparsely supplied by immunoreactive fibers. Occasional cell bodies were stained in the myenteric plexus. Staining was abolished by preabsorption of the primary antibody with APM. APM was characterized in membranes prepared from the muscle and mucosa of the guinea pig and rat stomach, small intestine, and colon by Western blotting. The major immunoreactive protein identified in membranes prepared from all tissues had an apparent molecular weight of 140, corresponding to the monomer of APM. In the brush border APM has a digestive function, whereas in neural tissue it may degrade and inactivate neuropeptides.     

Selective damage of intrinsic calcitonin gene-related peptide-like immunoreactive enteric nerve fibers in streptozotocin-induced diabetic rats

The distribution of calcitonin gene-related peptidelike immunoreactive (CGRP-LI) nerve fibers in the myenteric plexus of ileum and proximal colon of rats 8 wk after induction of diabetes with streptozotocin was studied using immunohistochemical techniques. A marked decrease in CGRP-LI nerve fibers mainly around the ganglion cells of the myenteric plexus of both ileum and proximal colon was observed in diabetic rats. The sparsely located immunoreactive nerve cell bodies in the control rats were absent in the diabetic preparations. There were, however, intensely stained CGRP-LI varicose nerve fibers that ran through the internodal strands and over the myenteric ganglia of the diabetic intestines. These findings indicate the presence of CGRP-LI nerve fibers of dual origin in the intestinal wall. The absence of positive cell bodies and diminished CGRP-LI nerve fibers around the ganglion cells in the diabetic tissues suggest that the state of diabetes selectively affects CGRP-LI nerve fibers of intrinsic rather than extrinsic origin. Furthermore, the absence of change in substance P-like immunoreactivity in the enteric system of rats with streptozotocin-induced diabetes of the same duration suggests that calcitonin gene-related peptide and substance P are contained in different populations of intrinsic nerve fibers in the gastrointestinal tract of the rat.     

Nitric Oxide Synthase (NOS) Expression in the Myenteric Plexus of Streptozotocin-Diabetic Rats

Nitric oxide (NO) is an important inhibitoryneurotransmitter in the gut. Alterations in NO mediatedresponses have been described in diabetic animals. Thepresence of nitric oxide synthase (NOS) reflects the potential for NO synthesis and is found inneurons in the myenteric plexus. The aim of this studywas to determine changes in nitric oxide synthase (NOS)expression in the myenteric plexus of thegastrointestinal tract of diabetic rats at three months ofstreptozotocin-induced diabetes, compared to age matchedcontrols, using immunohistochemistry. Diabetic animalsshowed a decrease in NOS expression in the antrum, with 59.1 ± 7.3% of neurons beingpositive for NOS in diabetes compared to 81.2 ±4.7% in controls (P < 0.05). NOS expression induodenum, ileum, and colon of diabetic animals was notstatistically different from controls. Decreased expression of NOS inantrum may contribute to altered gastric emptyingobserved in diabetics.     

Ginkgo biloba (EGb 761) Extract: Effects on the Myenteric Plexus of the Large Intestine in Wistar Rats

The objective of this study was to evaluate the effect of the purified extract of the Ginkgo biloba (EGb 761) plant on the myenteric plexus in the proximal and distal colon of Wistar rats for a period of 120 days. The experimental rats were divided into two age groups: a young group, sacrificed at age 90 days, and an adult group, sacrified at age 210 days. We observed a significant reduction in the number of neurons in the myenteric plexus of the adult group compared to the young group in both of the segments studied (P < 0.01). The adult group treated with Ginkgo biloba showed a significant increase in neuronal profile area in both the segments studied (P < 0.001). It can be concluded from these results that treatment with the purified Ginkgo biloba (EGb 761) plant extract at a dose of 50 mg/kg body weight has neurotrophic effect on the myenteric plexus in the proximal and distal colon of rats after 120 days of treatment.     

Differential effect of streptozotocin-induced diabetes on the innervation of the ileum and distal colon

The effect of short-term and long-term streptozotocin-induced diabetes on the pattern of distribution and tissue content of adrenergic and peptidergic nerves in ileum and distal (descending) colon of the rat was examined using immunohistochemical, biochemical, and immunochemical techniques. The effect of short-term streptozotocin-induced diabetes on the level of noradrenaline compared with weight-restricted (starved) and untreated controls in the celiac (celiac-superior mesenteric ganglia complex) and inferior mesenteric ganglia, which supply the two regions of the intestine, was also compared. The pattern of change in the distribution of dopamine-beta-hydroxylase-, substance P-, calcitonin gene-related peptide-, and vasoactive intestinal polypeptide-like immunoreactive nerve fibres that was observed in the ileum from diabetic rats was not evident in the myenteric plexus of distal colon. In contrast to the ileum, there was no evidence of degenerative change in any of the nerve types investigated in the myenteric plexus of the distal colon. The level of vasoactive intestinal polypeptide in the diabetic rat ileum was significantly increased, whereas the level of noradrenaline was reduced; no such changes were observed in the distal colon. The tissue content of noradrenaline in the celiac ganglion, which projects to the ileum, was increased at 8-week diabetes compared with both weight-restricted and untreated controls, whereas the diabetic state had no effect on the levels of noradrenaline of the inferior mesenteric ganglion, which projects to the distal colon. It is concluded that there is a differential effect of streptozotocin-diabetes on different regions of the rat intestine. The adrenergic and peptidergic innervation of the distal colon were changed little compared with ileum. This may be explainable in terms of the different functional roles of these two regions of the intestine and/or by the difference in origin of the sympathetic nerves supplying the two regions of the intestine.     

Spontaneous diabetes in eSS rats

Summary A spontaneous non-insulin-dependent diabetes in a highly inbred line of rats called eSS has been described. It is characterized by early impaired glucose tolerance worsening with age. Males are far more severely affected than females. These animals also exhibit hypertriglyceridemia and hypercholesterolemia. In spite of their hyperglycemia, eSS males have an excess of circulating plasma insulin compared with α controls. Eight-month-old eSS males were sensitive to exogenous insulin. Moreover, as the plasma insulin values decrease with age, glucose tolerance is further impaired. An improvement in the metabolic disturbances was registered in diabetic eSS males under long-term food deprivation. Histopathological examination of the pancreas revealed marked changes compared with age-matched controls. The pancreatic islet structure looked disrupted and islets became smaller and more scattered with advancing age. A diffuse glomerulosclerosis, interstitial lymphocyte infiltrates and tubular nephrosis were present in kidneys.     

大鼠泻剂结肠肠壁神经生长因子受体p75的表达及其意义

背景：神经生长因子（NGF）及其受体与肠神经系统关系密切，演剂结肠有肠壁神经丛损害，但NGF受体p75在泻剂结肠中的表达和作用尚不明确。目的：研究NGF受体p75在正常大鼠和泻剂结肠大鼠中的表达及其在泻剂结肠形成中的意义。方法：采用大黄和酚酞建立泻剂结肠大鼠模型，以墨汁推进试验测定其传输功能：采用免疫组化法对正常大鼠和泻剂结肠大鼠的结肠肠壁进行p75检测。观察其在肠壁中的分布和表达情况。结果：与对照组相比，模型组肠道传输功能明显减慢，大黄组和酚酞组黑染肠管长度和百分比（黑染肠管长度／肠管总长度）均较对照组显著减低（P〈0．01，P〈0．05）。p75存正常大鼠结肠黏膜下神经丛中呈阳性表达，在肌间神经丛中多呈弱阳性表达。大黄组中p75表达明显增强，黏膜下神经丛亦呈强阳性表达，与对照组相比有显著差异（P〈0．01）；肌间神经从中多呈阳性表达（P〈0．05）。酚酞组黏膜下神经丛呈阳性表达，肌间神绎丛3只呈阳性表达，余表现为弱阳性或阴性，与对照组相比无明显差异。结论：p75在泻剂结肠中的异常表达可能参与肠神经丛冲经元细胞的退化变性或凋亡．从而引起泻剂结肠的肠神经系统病理变化，进一步导致结肠动力异常。这种损害与长期应用刺激性泻剂有关。     

Ucn3及其受体CRFR2在肠易激综合征大鼠模型肠神经系统中的表达

目的:探讨尿皮质素3(Urocotin3,Ucn3)及其受体促肾上腺皮质释放因子受体2(corticotrophin releasing factor receptor2,CRFR2)在肠易激综合征中的表达.方法:将36只180-220g的Wistar大鼠随机分为对照组(N)、急性应激组(A,急性束缚1h)、慢性应激组(C,28d不可预知轻度应激)、急慢性联合应激组(AC,在慢性应激基础上给予急性束缚)4组建模.采用排便粒数、敞箱行为评分和蔗糖水偏嗜度评价动物模型.建成后留取大鼠结肠组织,采用Real-timePCR方法检测各组大鼠结肠中Ucn3及其受体CRFR2表达水平的变化.结果:Ucn3在各组大鼠结肠中的表达:N组1.108±0.293,A组3.594±1.839,C组1.852±0.674,AC组3.989±1.591,各应激组Ucn3的表达均高于对照组(P<0.05),各应激组间A组vsC组(P<0.017),C组vsAC组(P<0.002),表达有统计学差异.CRFR2在各组大鼠结肠中的表达:N组1.042±0.217,A组2.119±0.468,C组1.568±0.507,AC组2.392±0.840,各应激组CRFR2的表达均高于对照组(P<0.05).各应激组之间没有统计学差异.结论:慢性应激、慢急性联合应激建立肠易激综合征大鼠模型重复性好.Ucn3及其受体CRFR2在肠易激综合征中表达升高,且Ucn3在急性应激后升高比慢性应激后更明显.     

糖尿病大鼠胃窦胆碱能神经元与胃动力障碍的关系

目的 探讨链脲佐菌素(STZ)-糖尿病大鼠胃动力障碍和胃肌间神经丛胆碱能之间的关系.方法 45只SD大鼠随机分为对照组、糖尿病组和胰岛素组.成模后16 w测定大鼠胃动力,观察胃肌间神经丛胆碱能神经元的形态变化.结果 与对照组比较,糖尿病组大鼠胃动力减弱(P<0.01),胃窦肌间神经丛胆碱能神经元计数显著降低(P<0.01).与糖尿病组相比较,胰岛素组胃动力显著增高 (P<0.05),胃窦肌间神经丛胆碱能神经元平均光密度显著增高(P<0.05),胆碱能神经元计数有改善的趋势(P>0.05).结论 STZ-糖尿病大鼠胃动力障碍可能与胃肌间神经丛胆碱能神经损伤有关,胰岛素治疗能在一定程度上改善糖尿病胃动力障碍.     

肠道嗜铬细胞数量和5-羟色胺受体3表达在大鼠衰老过程中的变化及意义

目的 检测不同鼠龄SD大鼠肠道推进率、肠道黏膜嗜铬细胞数量和肠肌间神经丛5-羟色胺受体3(5-HT3R)的表达,探讨生理性衰老过程中肠道运动功能变化的规律及其机制. 方法 80只健康SD大鼠分为3月龄、9月龄、18月龄、24月龄及30月龄5组,每组各16只.以印度墨汁为标记物,检测大鼠的肠道推进率;采用免疫组化链霉亲和素-生物素-过氧化物酶复合物(SABC)法染色,检测大鼠空肠、回肠和结肠黏膜及黏膜下嗜铬细胞的数量以及肠肌间神经丛5-HT3R的表达.结果肠道推进率30月龄组大鼠为(52.1±9.8)%,明显低于3月龄组(67.2±13.5)%(t=7.013,P=0.001);30月龄组大鼠空肠、回肠及结肠黏膜和黏膜下嗜铬细胞数量分别为(11.1±3.0)个、(10.6±1.9)个和(10.2±4.3)个,较3月龄组(22.9±6.2)个、(25.8±7.1)个和(23.0±5.7)个减少(t=3.640,t=3.384,t=4.154,均为P<0.01);大鼠空肠和结肠的5-HT3R表达30月龄组分别为4.8±1.4和9.3±4.2,较9月龄组的8.9±1.5和14.5±5.3减少(t=3.464,t=3.003,均为P<0.01),回肠5-HT3R 30月龄组和3月龄组分别为5.0±1.3和9.0±1.7(t=4.549,P<0.001). 结论 老年大鼠肠道推进率、肠道嗜铬细胞数量及肠肌间神经丛5-HT3R表达均显著降低,并随年龄增长而逐渐明显;老年大鼠肠道运动功能的明显下降与肠嗜铬细胞数量以及肌间神经丛5-HT3R的表达显著降低有一定的相关性.     

Myenteric plexus in streptozotocin-treated rats. Neurochemical and histochemical evidence for diabetic neuropathy in the gut

Adrenergic, cholinergic, and serotoninergic nerves were studied in the myenteric plexus of ileum and colon from streptozotocin-treated rats, an animal model of juvenile-onset diabetes. In view of clinical reports implicating diabetic autonomic neuropathy as the cause of gastrointestinal dysfunction in diabetes mellitus, neurochemical and histochemical techniques were used to study changes in the innervation of the gut. In the myenteric plexus of the ileum from diabetic animals, adrenergic nerves displayed signs of degeneration and the brightness of fluorescence in serotoninlike immunoreactive nerves was lower. Cholinergic nerves, however, did not display any signs of reduction in the ileum, and both choline acetyltransferase and acetylcholinesterase activities per centimeter were increased. In contrast, in the proximal colon 8 wk after induction of diabetes, neurochemical assays revealed significant increases in noradrenaline and serotonin levels as well as choline acetyltransferase activity, although no obvious changes in the pattern of innervation could be detected histochemically. The results indicate that changes do occur in the innervation of the gut of the streptozotocin-diabetic model shortly after the induction of diabetes, although they differ significantly in the ileum and colon; these may be of relevance to the types of gastrointestinal dysfunction displayed in human diabetes.     

Regional differences in the nitrergic innervation between the proximal and the distal colon in rats

Background & Aims: Functional differences in the inhibitory neural pathway between the proximal and the distal colon are unknown. Methods: We investigated the nonadrenergic, noncholinergic (NANC) relaxation, nitric oxide synthase (NOS) synthesis, and NOS messenger RNA (mRNA) expression of the myenteric plexus in the proximal and the distal colon in rats. Results: Transmural nerve stimulation of the neuromuscular preparations from the proximal colon showed greater NANC relaxations than those from the distal colon. NANC relaxations were abolished by the NO biosynthesis inhibitor (N^G-nitro-L-arginine methyl ester) in the proximal and the distal colon, suggesting mediation by NO released from the myenteric plexus. The average number of NOS-immunoreactive cells was significantly higher in the tissue from the proximal colon than in the tissue from the distal colon. Western and Northern blot analyses showed a higher density of the immunoreactive NOS band and the NOS mRNA band in the tissue from the proximal colon than in that from the distal colon. Conclusions: These observations indicate that the number of NOS-containing neurons and the NOS activity are increased in the myenteric plexus of the proximal colon compared with the distal colon, resulting in greater NANC relaxation in the proximal colon. These findings may explain the physiological role of the proximal colon as an organ for fecal storage and absorption of excess fluid.GASTROENTEROLOGY 1998;115:1504-1512     

糖尿病大鼠胃肠功能紊乱时结肠组织中Cajal间质细胞的表达

目的观察糖尿病大鼠胃肠功能紊乱时结肠组织内Cajal间质细胞的分布及表达变化,探讨Cajal间质细胞在糖尿病胃肠功能紊乱发病机制中的作用。方法30只SD大鼠随机分为两组,糖尿病组20只,正常对照组10只。糖尿病组大鼠用链脲佐菌素单剂量腹腔注射建立糖尿病模型,对照组注射等量枸橼酸缓冲液。两组大鼠饲养6周后处死,计算胃肠推进率并且收集结肠组织标本。用免疫组化方法观察Cajal间质细胞在两组大鼠结肠组织内的分布和表达,用W estern b lot方法检测c-k it蛋白在两组大鼠结肠内的表达。结果糖尿病组大鼠胃肠推进率较对照组明显降低（P〈0.05）。免疫组化和W estern b lot检测都显示糖尿病大鼠结肠组织内Cajal间质细胞的表达较正常大鼠明显减少（P均〈0.05）。结论糖尿病大鼠结肠组织内Cajal间质细胞表达减少,推测与糖尿病大鼠胃肠功能紊乱有一定相关性。     

Intestinal Anastomoses from Diabetic Rats Contain Supranormal Levels of Gelatinase Activity

PURPOSE: Early postoperative strength in intestinal anastomoses is reduced in diabetic rats, whereas collagen deposition is essentially unchanged, suggesting that increased matrix degradation may be the cause of diminished wound strength. The aim of this study was to investigate whether (gelatin-degrading) matrix metalloproteinase activity is enhanced in intestinal anastomoses from diabetic rats. METHODS: Sixty male young adult Wistar rats underwent resection and anastomosis of both ileum and colon. In half the animals diabetes was induced seven days before operation by streptozotocin injection (50 mg/kg intravenously). Gelatinase activities in extracts from uninjured intestine and anastomoses at one, three, or seven days after surgery were measured by quantitative gelatin zymography. RESULTS: After surgery, profound changes were observed with time for gelatinase activities with molecular weights of 50 and 60 kDa, thought to represent matrix metalloproteinase-2, and of 66, 80, 105, 140, 220, and 260 kDa, thought to represent various forms of matrix metalloproteinase-9. In many cases, specific activities were significantly (P < 0.05) higher in the anastomotic extracts from diabetic rats. Total anastomotic activities present at Day 7 were strongly elevated for most matrix metalloproteinase forms in ileum and colon from diabetic animals. CONCLUSION: Experimental diabetes leads to a sustained and elevated presence of gelatinase activity in intestinal anastomoses. Increased local matrix degradation may contribute significantly to impaired anastomotic strength in the intestine observed under this condition.     

Myxedema megacolon after external neck irradiation

Myxedema megacolon is a rare manifestation of hypothyroidism. It may respond to appropriate treatment but is sometimes irreversible, resulting in fatal complications. Two possible mechanisms to explain the colonic atony include (1) myxomatous infiltration of the submucosa with separation of the muscular fibers from the ganglia of Auerbach's plexus, and (2) severe autonomic neuropathy affecting the extrinsic nerves to the colon and the myenteric plexus. Histology from our case supports the first proposed mechanism. Urecholine challenge and manometric measure response may help predict reversibility of colonic atony. Treatment should be individualized and should include factors such as age, duration of symptoms, and other medical illness. Low-dose oral or intravenous triiodothyronine is effective. Hypothyroidism following external radiation of the neck for lymphoma is not uncommon, and the risk increases following one or more lymphangiograms. Such patients should be followed up with regular TSH estimations for at least three years.     

肝衰竭大鼠胃窦胆碱能和氮能神经分布的变化分析

目的观察肝衰竭大鼠胃排空及胃窦肌间神经丛胆碱能和氮能神经的变化。方法 40只Wistar大鼠随机分为肝衰竭模型组和对照组,采用葡聚糖蓝-2000为标志物观察大鼠胃排空的变化,应用乙酰胆碱酯酶(AchE)和还原型辅酶Ⅱ硫辛酰胺脱氢酶(NADPH-d)组织化学染色及肌间神经丛全层铺片技术,观察肝衰竭大鼠胃窦肌间神经丛胆碱能和氮能神经的变化,并进行定量分析。计量资料以均数±标准差(x±s)表示,组间比较采用t检验。结果肝衰竭组大鼠胃排空明显减弱(163.00±25.68 vs 100.00±18.93,P0.01),胃窦肌间神经丛胆碱能阳性神经元数量减少,神经纤维变细,分布较稀疏,明显低于对照组(t=3.201,P0.01);氮能神经阳性神经元数量及神经纤维分布明显高于对照组(t=2.912,P0.01)。结论肝衰竭大鼠胃功能的减退与胃窦肌间神经丛胆碱能神经分布减少及氮能神经分布增加有关。     

Impaired nitrergic innervation in rat colitis induced by dextran sulfate sodium

BACKGROUND & AIMS: The pathophysiological role of neuronal nitric oxide synthase (nNOS) in colitis remains unknown. METHODS: We investigated colonic transit, nonadrenergic, noncholinergic (NANC) relaxation, nNOS activity, and nNOS synthesis in the myenteric plexus in dextran sulfate sodium (DSS)-induced colitis in rats. RESULTS: Oral administration of 5% DSS for 7 days induced predominant distal colitis and delayed colonic transit. In the proximal colon, carbachol-, sodium nitroprusside-, and electrical field stimulation (EFS)-induced responses were not different between control and DSS-treated rats. In the distal colon, EFS-evoked cholinergic contraction, NANC relaxation, and orphanin FQ-induced contraction were significantly impaired in DSS-treated rats compared with those in control rats, but carbachol- and sodium nitroprusside-induced responses remained intact in DSS-treated rats. The number of nNOS-immunopositive cells, catalytic activity of NOS, and nNOS synthesis in the colonic wall were significantly reduced in the distal colon of DSS-treated rats. In contrast, the number of PGP 9.5-immunopositive cells and PGP 9.5 synthesis in the colonic wall remained intact in the distal colon of DSS-treated rats. CONCLUSIONS: These results suggest that impaired NANC relaxation in the distal colon is associated with reduced activity and synthesis of nNOS in the myenteric plexus in DSS-induced colitis.     

Morphology of myenteric plexuses in the human large intestine: comparison between large intestines with and without colonic diverticula

BACKGROUND: Large intestines with diverticula exhibit functionally abnormal peristaltic activity and elevated luminal pressure that may indicate functional changes in the myenteric plexus; however, no studies have investigated the characteristics of either normal or diverticula myenteric plexuses. METHODS: Tissue specimens obtained from 93 colorectal cancer patients without diverticula, 14 patients with perforated diverticulitis, and 12 colorectal cancer patients with asymptomatic diverticula were included in this study. Myenteric plexuses and ganglion cells were counted per centimeter, and the area and maximum diameter of the nuclei of ganglion cells were measured using an image analyzer. RESULTS: The number of myenteric plexuses and ganglion cells per centimeter was significantly higher in the descending colon, sigmoid colon, and rectum than in the cecum, ascending colon, and transverse colon. The area of the nuclei of ganglion cells was significantly larger in the descending colon and sigmoid colon than in the cecum and ascending colon. Compared with large intestines without diverticula, the number of myenteric plexuses was significantly higher in large intestines with diverticula, whereas the number of ganglion cells decreased in both right-sided and left-sided large intestines with perforated diverticulitis or asymptomatic diverticula. The area of the nuclei of ganglion cells was significantly smaller in large intestines with diverticula. CONCLUSION: The morphology of myenteric plexuses and the ganglion cells differs significantly among segments of the human large intestine. Large intestines with diverticula had significantly more plexuses but significantly fewer ganglion cells than large intestines without diverticula. The area of the nuclei of ganglion cells was also significantly smaller in large intestines with diverticula. Further studies are required to clarify how these changes are related to intestinal function and how they are involved in the etiology of diverticulosis.